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Chapter IV

Contents

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-


80

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

The number of military cases of this group of diseases which occurred in World War II turned out to be few indeed, but besides the reasons already given that these few cases deserve attention here is that research initiated and promoted by the Preventive Medicine Division, Office of the Surgeon General, and the Army Epidemiological Board (Board for the Investigation and Control of Influenza and Other Epidemic Diseases in the Army), contributed materially to the addition of knowledge about these important infections 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 4 million.l In this group, 27 deaths occurred, giving a case fatality ratio of about 17 percent. The chances that a large percentage of these cases were examples of encephalitis lethargica are good. However, as the etiological agent of that disease was never established, one cannot speak with any confidence that it was actually a virus disease and therefore deserves discussion here. Furthermore and fortunately, the incidence of encephalitis lethargica began to decline in the midtwenties, both in the United States and in 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 that other new types of encephalitis were soon to supplant Von Economo's disease.

It was during the 1930's that the arthropodborne virus encephalitides came under scrutiny, the first recognition of any member of the group being that of the virus of western equine encephalomyelitis, isolated with some difficulty, from a sick horse in 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 the World War. Washington: Government Printing Office, 1925, vol. XV, pt. 2, pp. 90-138, 656.


81

Rockefeller Institute of Medical Research at Princeton, N.J., found that strains of the equine encephalomyelitis viruses could be separated into eastern and western types. The "disease" for which these viruses were responsible was regarded at that time primarily, if not entirely, as one of horses. A manifest interest by the Army in this matter accompanied the report in 1934 by Lt. Col. (later Brig. Gen.) Raymond A. Kelser, VC, that these viruses could 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 of illness affected man. In 1933, a severe outbreak of human encephalitis occurred in and about the city of St. Louis, Mo. More than 1,000 human cases were reported with about an 18 percent mortality. The virus of St. Louis encephalitis was isolated in this epidemic more or less coincidentally by Drs. Ralph S. Muckenfuss and L. 'I'. Webster. Although sick horses received little notice during this epidemic, some of the investigators, including Maj. (later Brig. Gen.) James S. Simmons, MC, thought that St. Louis encephalitis might be related to one of the equine encephalitides and attempted to infect horses with the St. Louis virus. The assumption was correct, and the failure to substantiate it experimentally at that time might have been due to the fact that the horses used were from the St. Louis area and they could well have been immune to the disease.

It was also at about this time (1933-34) that U.S. investigators began seriously to compare the St. Louis epidemic with the existing situation in Japan where endemic encephalitis had appeared in parts of the home islands almost every summer since 1871. In 1924, there had been a particularly bad epidemic, and clinical studies had made, it possible for the Japanese to distinguish their diseases from epidemic encephalitis of the so-called A type (Von Economo's disease). For this reason, Japanese epidemic encephalitis has been termed type B encephalitis. The epidemic of 1924 had spread through wide area resulting in a heavy mortality among 6,000 reported cases. During the period from 1924 to 1937, outbreaks occurred almost every summer in Japan, resulting in a total of some 21,000 reported cases for that period with the heaviest concentration of cases occurring in the region of the Inland Sea. Similar recurrent appearances of summer or autumn encephalitis were known to have been reported from the Ryukyu Islands, as well as from Formosa Manchuria, and the far eastern maritime districts of Soviet Russia. Opinion in Japan was divided as to the means of spread, and by 1938, although one group had suspected that it was mosquitoborne, the balance of Japanese medical opinion held to the view that it was spread from the respiratory tract.

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


82

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

Early in the 1940's, information about these diseases was accumulating at a rather rapid rate, although much of it was still theory. Birds had been found to be infected, which made the epidemiological picture still more complicated. Eventually, the epidemiology of some of this group of diseases, as they occurred in the United States, was worked out largely through the efforts of Dr. William McD. Hammon at the University of California, San Francisco. From his work, the concept gradually emerged that, in this 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, and other animals were what might be called casual, though spectacular, accidents. Apparently, the avian infection could be very widespread numerically but was mild, 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 through the agency of Culex mosquitoes.

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


83

Canadian Army.2 It hardly could be questioned in the autumn of 1941 that here was a new disease of potential military importance to U.S. troops.

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

Clinical records from civilian as well as military medical practice indicate that the diagnosis of encephalitis is commonly made whenever clinical manifestations suggestive of cerebral disturbance (ranging from mild lethargy to coma, from slight delirium to complete disorientation, from restlessness to convulsions) are associated with an otherwise undiagnosable febrile illness. The diagnosis is not infrequently made when the syndrome of aseptic meningitis is associated with what may be interpreted as lethargy or unusual restlessness. It is made not only when the cerebral disturbance is associated with pleocytosis, but also in its absence, and indeed not infrequently when toxic encephalopathy is associated with certain bacterial infections.

In the period 1941-46, and subsequently, the exact method of making a diagnosis of this group of virus diseases was by immunological and virological tests. Some of these became available during and immediately prior to World War II. However, the utilization of these tests, which included neutralization or complement fixation tests on matched specimens of sera, was more or less in its infancy and hardly more than half a dozen laboratories in the United States capable of carrying them out.4

Experience During World War II

Most, although not all, of the apprehension about arthropodborne virus encephalitides proved to be unnecessary, for when the Second World War was over the incidence of these infections in military personnel turned out to be small. There were no large wartime epidemics in the United 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 of recognized cases, incidence rates, and deaths ascribed to encephalitis is listed in tables 10 and 11. It is clear that the figures suffer somewhat from the inaccuracies of diagnoses which are apt to beset all figures on the incidence of the encephalitides, infectious or otherwise. As just mentioned, Sabin has pointed out that the clinical diagnosis of any kind of encephalitis 

2Report, Commission on Neurotropic Virus Diseases, Board for the Investigation and Control of Influenza and Other Epidemic Diseases in the Army, 1 Dec. 1941-1 May 1942.
3Sabin, Albert B.: Encephalitis. In Medical Department, United States Army. Preventive Medicine in World War II. Volume VII. Communicable Diseases: Arthropodborne Diseases Other Than Malaria. [In preparation.]
4Better known laboratories readily available to the Medical Department of the U.S. Army for the diagnostic purpose of these diseases, in 1941-45, included that of the Army Medical School, Washington, D.C., the G. W. Hooper Foundation of the University of California in San Francisco, the Rockefeller Institute for Medical Research in New York City (both of which facilities were made available through the Commission on Neurotropic Virus Diseases of the Army Epidemiological Board), and a few other laboratories, also connected with the Army through that Board.


84

without the assistance of serological tests is notoriously difficult. In view of the fact that such immunological tests were not available in many of the cases occurring in military personnel during wartime, the data in tables 10 and 11 must be regarded as being approximate rather than definitive. It should be noted, however, that the rates for infectious encephalitis were higher in 1944 and 1945 in the Pacific than in Europe. This is what should have been expected because, except for the presence of tickborne Russian spring-summer encephalitis in Czechoslovakia and in eastern Austria, the arthropodborne encephalitides as they are now known to occur in man are almost entirely absent from Europe.

TABLE 10.-Admissions for encephalitis 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


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

NOTE.-Figures in parentheses are subtotals.


85

TABLE 11.-Deaths due 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 medical records] 
[Rate expressed as number of deaths per annum per 100,000 average strength]

Diagnosis and area


1942-45

1942

1943

1944

1945


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 as well as other types of infectious encephalitis. Excludes lymphocytic choriomeningitis.
2Includes postvaccinal encephalomyelitis. 
3Data are not available.
4Includes encephalomyelitis, other and undetermined. Excludes lymphocytic choriomeningitis.

NOTE.-Figures in parentheses are subtotals.

No sizable epidemic due to one of the known encephalitic viruses was ever recorded in U.S. Forces stationed within the United States during the period 1942-45. However, a possible outbreak, of which the agent was never identified, occurred during the summer of 1941, when 12 mild cases of encephalitis developed in a force of unknown size maneuvering near Sabinal, Tex.5 Sporadic cases of proved arthropodborne virus encephalitides occurred in western training areas during 1942-45, but the incidence never reached anything comparable to that experienced by the Canadian troops in Manitoba in 1941. Clinical descriptions of these sporadic cases in U.S. troops apparently did not differ from the usual textbook descriptions, and no unusual findings are known to the author.

Outside the confines of the United States, a single case due to one of the exotic 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 Sam Houston, Texas. J.A.M. A. 120: 358-361, 3 Oct. 1942.


86

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

By far the most important group of cases, however, which occurred during the Second World War took place in an oversea theater. This was the small but important outbreak identified as Japanese B encephalitis which involved both natives and troops on the island of Okinawa in the summer of 1945.

In the spring of 1945 and at the time of the occupation of islands north and northwest of Guam, the Medical Department recognized that U.S. troops were entering territory where Japanese B encephalitis might be endemic. For this reason, knowledge of the disease was summarized for use by medical officers in War Department Technical Bulletin (TB MED) 181, July 1945. Japanese B encephalitis had been previously reported as recurring not only in Japan proper but in the Ryukyu Islands, Formosa, Korea, eastern China, in certain of the 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 of encephalitis within all these areas.

The epidemic occurred during a combat period on the island of Okinawa and has been well described by Sabin,7 so that his account need 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 April 1945, and during the entire spring and early summer months, fighting continued sporadically on the island. Encephalitis first appeared among the native population early in July. The first native patients with severe encephalitis observed 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 of Okinawa. During the following 3 months, 127 patients were seen by military government medical facilities on the two islands; 66 of the 91 patients found on Okinawa were admitted to the isolation hospital for observation and treatment. The etiological agent of the disease was first established by the results of complement fixation and neutralization tests and by recovery of the virus from a fatal case.

Two groups of workers participated in these identifications. The civilian cases were first identified by Hodes, Thomas, and Peck,8 of the Naval Medical Research Unit No. 2, then established on the island of Guam, 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 in recognizing clinically and,

6Randall, R., and Mills, J. W.: Fatal Encephalitis in Man Due To Venezuelan Virus of Equine Encephalomyelitis in Trinidad. Science 99: 225-226, 17 Mar. 1944.
7(1) Sabin, A. B.: Epidemic Encephalitis in Military Personnel; Isolation of Japanese B Virus on Okinawa in 1945; Serologic Diagnosis, Clinical Manifestations, Epidemiologic Aspects and Use of Mouse Brain Vaccine. J.A.M.A. 133: 281-293, 1 Feb. 1947. (2) See footnote 3, p. 83.
8Hodes, H. L., Thomas, L., and Peck, J. L.: Cause of an 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.


87

subsequently, in identifying the etiology of Japanese B encephalitis was accomplished under arduous combat conditions and was indeed a noteworthy event, both in military medicine and in the history of this disease in general. At the time the disease was discovered, the island was the most important advanced base in the Pacific area. Large forces of U.S. troops were already assembled for the projected invasion of the home islands of Japan scheduled for the autumn. It was reasonable to assume that these troops were and would be susceptible to neurotropic virus disease to which they had never been previously exposed, and the danger of an epidemic was therefore a matter of great concern to the Medical Departments of the Army and the Navy. The news of the epidemic of "a dread Japanese brain disease" on Okinawa had also spread among the troops with demoralizing effect.

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

Mosher11 has described how the situation was handled on Okinawa in July and August 1945. The investigation of encephalitis was assigned to the Military Government Research Center, and on 18 July 1945, an isolation hospital for the study of the disease was opened at Gimbaru. By direction of the commandant of the U.S. Military Government, all native patients with cerebrospinal symptoms suggestive of encephalitis were referred to the 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 in some areas native police assisted in finding the sick. A visiting nurse program was instituted by some of the dispensaries. While these nurses were largely untrained volunteers, they facilitated in some degree in case finding and in referral of cases to the hospitals. Between early July and October, a total of 91 natives of Okinawa

10Tigertt, W. D., and Hammon, W. McD.: Japanese B Encephalitis: A Complete 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 the 1945 Outbreak on Okinawa. U.S. Nav. M. Bull. 47: 586-593, July-August 1947.


88

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

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

In a report of the outbreak by Lewis and his associates,12 which represents perhaps the first 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. military personnel, as observed both on Okinawa and subsequently in Korea, have been well documented in War Department Technical Bulletin (TB MED) 181 on Japanese B encephalitis, issued on 6 April 1947.

Although the clinical features of Japanese B encephalitis do not seem to differ materially from those of St. Louis encephalitis and western equine encephalomyelitis, which were already in 1945 well described in U.S. textbooks of medicine, it may be worthwhile to mention something here of the clinical picture of Japanese encephalitis as it appeared on Okinawa. Most important for diagnostic purposes was the appearance of the following signs during the course of an acute febrile illness: Mental confusion, disorientation, purposeless movements, speech disturbances, and complete aphasia. Varying degrees of lethargy might be present ranging from abnormal somnolence to complete coma in patients who also exhibited high fever and nuchal and spinal rigidity. As a rule, there was a period of 2 or 3 days before the appearance of any signs suggesting involvement of the nervous system. During this time, headache and low-grade fever were the only symptoms. Generalized convulsions of the grand mal or petit mal type were occasionally the first signs of involvement of the nervous system, with stiffness of the neck and back, and other signs already mentioned, coming later. Flaccid paralysis, suggesting involvement of large numbers of lower motor neurons in the spinal cord or medulla, was not seen. Localized spastic paralysis was seen only once among 15 patients, although generalized rigidity was present in the more severe cases. Dissociated eye movements were seen in only one patient, and diplopia did not occur. Pupils were usually contracted and reacted poorly to light; a sticky exudate was not infrequently seen about the eyes. The reflexes were variable and by themselves of little aid in differential diagnosis. The abdominal reflexes were usually absent while the tendon reflexes were most exaggerated; only occasionally did they 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.


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As a rule, the fever lasted from 7 to 11 days. It was high after the appearance of nervous signs and frequently remittent, although it is uncertain to what extent the administration of antipyretics may have affected the temperature curve. A relative bradycardia was invariably present during the febrile phase with a pulse rate of about 50 to 60 being common after defervescence. In fatal cases, death due to encephalitis occurred within the first 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 after defervescence. Subsequently, it became apparent from observations by Japanese physicians and by neurological consultants from the United States that residual symptoms from this disease were noted in only a small percentage of patients.13 These did not grow progressively worse as in the sequelae in encephalitis lethargica.

As to laboratory findings in the blood and spinal fluid, during the acute phase of the disease, the white blood cells in the former were likely to be increased 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 all of the military patients whose illness was definitely proved to be due to this infection. The cells were, as a rule, predominantly mononuclear, although in at least two of the group polymorphonuclear leukocytes predominated; spinal fluid sugar and chloride were in the normal range. Protein was normal or only slightly increased early in the disease, while during convalescence a 3 or 4 plus Pandy reaction was not uncommon.

In American military personnel, poliomyelitis and "aseptic meningitis''14 offered the greatest problems of clinical differential diagnosis. Among the children and natives of older age groups, tuberculous meningitis proved to be another important differential diagnostic consideration. Of aid in the diagnosis was the use of neutralization and complement fixation tests and virus isolation from fatal cases. It was fortunate indeed that, during the

13During World War II, and when this disease was first encountered, a subject of great interest was whether the military cases of Japanese B encephalitis would result in any residual deficiencies in nervous function after the acute stage of the disease had been passed successfully. This was a matter which should call for preferably long-term followup observations. One postwar study which can be mentioned is embodied in a report to the Surgeon General's Office by Dr. Charles D. Aring, Professor of Neurology, University of Cincinnati, Ohio, made under the auspices of the Army Epidemiological Board in 1948 (published in Arch. Neurol. & Psychiat. 62: 759-765, December 1949). Dr. Aring examined 19 late cases of Japanese 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 suffering from residua, and even in this case it seemed probable that the signs were attributable to an emotional disorder apart from his recent acute disease. It was Dr. Aring's opinion that once the "dangerous period" had been passed without the appearance of crippling neurological signs, the patient would go on to good recovery, with the possible exception of the development of parkinsonism, which had been reported in Japanese cases as an occasional occurrence.
14Several years later, it was shown that leptospirosis was the cause of at least one outbreak of "aseptic meningitis" in troops on the island of Okinawa.


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

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

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

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

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

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

In summary, therefore, and in retrospect, it would appear that during World War II after considerable preparation with regard to the arthropodborne virus encephalitides this group of diseases turned out to be less of a threat as a military disease than had been anticipated, but in this respect there was feeling that the Armed Forces had been lucky. In any event, considerable was learned about arthropodborne virus encephalitides which constituted a group of what might be called new diseases as far as the Medical Departments of either the Army or the Navy were concerned. The first contact by American troops with a most important member of this group, namely, Japanese B encephalitis, 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.: The Topographic Distribution of Lesions in Central Nervous System in Japanese B Encephalitis; Nature of the Lesions, With Report of a Case on Okinawa. Arch. Neurol &. Psychiat. 57: 673-692, June 1947.
17See footnote 3, p. 83.


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in the military history of virus diseases. That the disease should have been promptly recognized, and the agent isolated by medical officers from the Army and the Navy working close to the combat areas, was a noteworthy achievement. Subsequent to World War II, important additions were made to knowledge about this disease, as a result of experiences in the army of occupation in Japan,18 but the introduction to this story came in July and August of 1945 on the island of Okinawa.

POLIOMYELITIS

Just prior to the onset of World War II, it was generally agreed by medical officers in the Army that poliomyelitis was not a disease of military significance. This was based on the very low incidence of poliomyelitis in 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 not exclusively, 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 opinion needed revision, for although the number of cases of poliomyelitis which had occurred in the Army during World War II was not very great (in the neighborhood of about 1,000 covering the 4 war years), the disease had been responsible for many problems. The degree of crippling was high; the percentage of bulbar cases was high; the mortality was high; and the element of panic which poliomyelitis caused, either in outbreaks or in single cases within military units, had proved to be appreciable. Not only had this been so within the confines of the United States but, with the exception of the European Theater of Operations, U.S. Army, the incidence of poliomyelitis had been considerably greater in troops abroad than at home (p. 99).

The statistics with regard to the prevalence of poliomyelitis in U.S. Army personnel preceding and during World War II have been admirably

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

Also during the summer of 1946, an outbreak of illness among U.S. Marines stationed in Tientsin, China, which at first was thought to be encephalitis and later regarded as poliomyelitis, led to certain investigations by Sabin and his coworkers (Proc. Soc. Exper. Biol. & Med. 65: 183-187, June 1947) which revealed that extensive previous inapparent infection with Japanese B encephalitis virus existed among the populations of Shanghai and Tientsin, where no epidemics of encephalitis had been observed. The survey method employed by Sabin was one which had been followed by Japanese in Japan and elsewhere, for some years; namely, by determining the presence or absence of neutralizing antibodies for the virus of Japanese B encephalitis in large numbers of sera collected from various age groups of the local population living in various locations. It was, however, one of the first of many subsequent examples of the use of the serological antibody survey by U.S. investigators as a means of outlining the geographic distribution of epidemic encephalitis in what might be called unknown territory.


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CHART 2.-Seasonal incidence of poliomyelitis in the Army in the continental United States compared with contemporaneous civilian rates during the second half of each year, 1943-46

 

reviewed by Sabin in another volume in the history of the Medical 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 at the expense of reiteration because they represent new information about this disease acquired as a result of military experience. Primarily, it became apparent during the years 1941-45 that men of military age, born and brought up in the United States during the 1920's and 1930's, were more susceptible to poliomyelitis than their fathers had been in 1917-18. This was unexpected. The military rates for 1943-46 within the United States

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


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

Another point that came out of the military experience was that in 1941 there was little appreciation that poliomyelitis could be a tropical disease of any importance, or that it amounted to much in subtropical areas. Local civilian public health statistics within the great majority of tropical areas had for years reported a dearth of epidemics and a very low incidence of poliomyelitis in the native-born inhabitants.20 Therefore, it was naturally thought that this disease should not be of particular danger to troops in such areas. It was not long, however, before it became apparent that poliomyelitis could exist in poorly sanitated tropical or subtropical areas as a hidden disease, hitherto unsuspected. Later, by the copious use of hindsight, one could surmise that this might have been predicted on the basis of prewar experience with poliomyelitis in the Philippines. As early as 1936, Lt. Col. (later Brig. Gen.) Charles C. Hillman, MC, had reported an interesting observation. which was to be repeated frequently during World War II. In his account21 of an outbreak of poliomyelitis which occurred in Manila, Philippine Islands, in 1934, he described 17 patients with poliomyelitis who were admitted to the Sternberg General Hospital in Manila; of these, 3 cases were in military personnel, the remaining 14 being in dependents. Coincidentally, the number of cases in the local Philippine civilian population was small, presumably represented by only nine cases. Colonel Hillman commented on the fact that, considering the vast preponderance of natives to American-born people in the community, there was indeed a striking discrepancy between the poliomyelitis incidence rate in the civilian population and that of the Americans. However, the extraordinary degree to which the immunity of the young adults in the two populations might differ was not appreciated at that time.

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

20Since 1945, many epidemics of poliomyelitis have been reported from tropical areas (Paul, J. R., Ramirez Corria, F., and Horstmann, D. M.: Analyses From a Tropical Epidemic of Poliomyelitis 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.


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The Surgeon General of the Army, the Division of Medical Sciences of the National Research Council sponsored a discussion by outstanding authorities in the field of poliomyelitis, which again resulted in a number of recommendations used by military officers. These recommendations are recorded by Sabin in another volume in the history of the Medical Department in World War II.22

Perhaps the first theater in which this disease became an appreciable problem was that of the U.S. Army Forces in the Middle East in 1943. Observations regarding the seriousness of poliomyelitis in British troops within the area during 1941-42 had already been made in 1943.23 The situation was later reviewed by Caughey and Porteous in a postwar report of their experiences which includes a description of an epidemic of poliomyelitis which had occurred in 1940-41 in New Zealand troops stationed in Egypt.24 Similar British observations were recorded in India with comments on the fact that poliomyelitis was particularly severe in foreign troops in India, whereas at the same time it seemed to be both uncommon and not severe in the natives there.

This early British experience in the Middle East was later shared by U.S. troops in North Africa, Egypt, and the Middle East generally during the summer of 1943. This joint experience has been described25 with particular reference to the high rate and high fatality of poliomyelitis in U.S. troops in contrast to its apparent rarity in the native adult Egyptians. Comment was also made on the absence of epidemics of poliomyelitis in the local native population and the fact that the only examples of the disease which did appear in the local population were in infants.

There was considerable difficulty with the diagnosis of poliomyelitis in U.S. troops stationed in this area during the summer of 1943. Medical officers had not been prepared for this disease and were very loath to accept suspicious cases as poliomyelitis. This may be understandable in that, at least at that period, the clinical picture of poliomyelitis in adults had received scanty treatment in American textbooks of medicine. At the 38th General Hospital near Cairo, Egypt, this author, in consultation, saw at least a dozen cases of poliomyelitis, several of which were fatal. In the majority of patients, the disease was characterized by insidious onset with 2 or 3 days of malaise, relatively little fever, but severe pain in the back. This is in some contrast to the textbook picture seen in children with an acute onset with fever and usually a biphasic course. Fortunately, at the 38th General Hospital, a virus laboratory 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, December 1943.
24Caughey, J. E., and Porteous, W. M.: An Epidemic of Poliomyelitis Occurring Among Troops in the Middle East. M.J. Australia 1: 5-10, 5 Jan. 1946.
25Paul, J. R., Havens, W. P., Jr., and Van Rooyen, C. E.: Poliomyelitis in British and American Troops in the Middle East; Isolation of the Virus from Human Faeces. Brit. M.J. 1: 841-843, 24 June 1944.


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mer of 1943. Monkeys were obtained locally and from Eritrea, where they had been trapped by members of the Army Veterinary Service, and the isolation of poliomyelitis virus by monkey inoculation with material from a number 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 fact that here, as elsewhere in areas remote from the United States, tank respirators and other respiratory aids were seldom available. As a result, poliomyelitis patients who developed severe respiratory paralysis promptly died. 

From the epidemiological standpoint, it was here in the Middle East that the idea first emerged that the phenomena which had been observed by Hillman in the Philippines in 1934 was one which could be repeated in a number of different areas, particularly in cities located in the tropics where sanitation was primitive. In other 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 the infection was almost universally acquired by natives in infancy and was almost universally unrecognized. Consequently, by the time the native child had reached the age of 2 or 3 years, he had had the disease (rarely in either paralytic or nonparalytic form), but commonly in inapparent form and had thus acquired some immunity. This immunity rate among the adult natives was high as opposed to the visiting troops from northern Europe, the United States, Canada, Australia, and New Zealand whose exposure to poliomyelitis at home had not been so heavy during infancy. When these troops entered these areas, poliomyelitis came to the surface, as it were, because of heavy exposure of a moderately susceptible population coming into an infectious environment. As a result, not only were appreciable numbers of cases of poliomyelitis acquired by the susceptible members of the "immigrant" troops, but small epidemics in U.S. troops were precipitated now and again of which notable examples appeared in 1944 and 1945 in the Philippines.

It would also appear that the same unsanitary conditions and proximity to native populations, which gave rise to high attack rates of bacillary dysentery and infectious hepatitis, were also associated with an increased incidence of poliomyelitis. Thus, poliomyelitis and these other diseases did not often occur among the troops in various primitive, tropical or subtropical, regions where the military installations were "beyond the range and influence of native villages." But where, as became particularly evident in the Southwest Pacific Area and in the Philippines, U.S. troops moved into the midst of congested native villages and towns with sanitation of the worst possible order, poliomyelitis appeared in unexpectedly high numbers of cases, along with the other infections whose etiological agents were known to occur predominantly in human feces.

26Report, Commission on Neurotropic Virus Diseases, Army Epidemiological Board, to Office of the Surgeon General, U.S. Army, May 1944, subject: Report of the Middle East Expedition of the Virus Commission.


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In the Philippine Islands, for instance, the story was typical. Prior to the invasion of the islands in 1944, the attacking force had spent a month on board ships without the appearance of a single case of poliomyelitis. But shortly after the occupation of Leyte began in October 1944, cases appeared, 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 an initial strength of about 200,000 to a little over 300,000 at the end of the year. In the next year, there were 245 cases (for all of 1945) in a force with an average strength of around 600,000. Sabin states that there is good reason to believe that this does not include all the cases. Studies on the disease here were reported by the virus team of the 19th Medical General Laboratory, Leyte.27 It was noted by them that there was no uniform history of the increase of upper respiratory infections in units involved, but several of the patients had had diarrhea or dysentery subsequent to arrival on Leyte. Nonparalytic cases were also recorded; several of them caused considerable difficulty in diagnosis. Coincidentally, no evidence of poliomyelitis appeared among the Filipinos so that in the Philippine Islands poliomyelitis was considered to be a disease of white people. In retrospect, the observations point to the fact that the local population in Leyte was the hidden reservoir of the virus.

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

Apart from the incidence of poliomyelitis in various oversea theaters, the incidence of poliomyelitis in troops in the continental United States was appreciable (chart 2). As a rule, most of the cases were sporadic examples of the disease which were not followed by outbreaks in the units in which they appeared. However, there were several small, sharp, and moderately serious epidemics in the United States during the period 1941-46. These epidemics have been discussed with care by Sabin in another volume in the history of the Medical Department in World War II.29

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

27Report, 19th Medical Service Detachment (General Laboratory), to Chief Surgeon, Headquarters, U.S. Army Services of Supply, Southwest Pacific Area, 28 Dec. 1944, subject: Poliomyelitis and Other Virus Diseases 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 the Poliomyelitis Epidemic in San Antonio, Tex., September-December 1942. [Official record.]


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among the families of officers and men stationed in that area, 11 of which were admitted to the Brooke General Hospital at Fort Sam Houston. This outbreak caused considerable concern locally and served as an illustration of the manner in which poliomyelitis can indirectly become a morale problem when it suddenly appears in the families of military personnel living on a large military post in this country.

A second outbreak, which was well described, occurred in a training unit designated as the STAR (Specialized Training and Reassignment) unit at Pasadena College, Pasadena, Calif. The STAR unit consisted of approximately 800 men among whom an explosive epidemic occurred in mid-August 1943, just after 310 of the men had left for duty at Indiana University, Bloomington, Ind. The first case, which ended fatally, occurred on the train, and subsequently, there were 16 other cases compatible with the diagnosis of paralytic or nonparalytic poliomyelitis in the group which went to Indiana. Among the men remaining at Pasadena 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 an isolated Army camp in the continental United States. Seventeen cases of paralytic poliomyelitis occurred within a brief period of 2 months, yielding a paralytic attack rate of approximately 0.57 per 1,000 men. All the cases were in soldiers.

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

The incidence of poliomyelitis among American troops in the European 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 of some significance within several theaters. This had been more or less unsuspected by medical officers, some of whom went to considerable lengths to determine whether the case of acute paralysis seen in North Africa, for instance, in 1943, might be due to some cause other than poliovirus. One of the reasons for the difficulties in making the diagnosis seemed to have been that at that time, in the mid-1940's, the average medical or pediatric textbook description of acute poliomyelitis described the picture of the juvenile case characterized with initial signs and symptoms of acute fever (often in two bouts), headache, vomiting, and stiff neck. Textbook descriptions of adult cases were few, and there was little awareness that adult cases could present a picture, quite different from the juvenile case, of insidious onset, often with little fever in the first few days and often with severe pain in the back. Consequently, it was with some reluctance that the diag-


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

Treatment

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

Considerable improvements were to be made in the decade following World War II in the development of various mechanical breathing aids for 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 Drinker respirator. This was a large, heavy piece of apparatus, bulky and difficult to transport. It was not standard equipment of many general hospitals. Nevertheless, a number of these tank respirators were available for hospitals in the United States, and occasionally, the emergency transportation of a tank respirator to a distant area was achieved. In retrospect and taking all things into account, it is not believed that loss of life due to the failure of availability of respiratory aids was a serious situation.

Oversea patients with residual paralysis were eventually evacuated to hospitals in the Zone of Interior where they could have orthopedic supervision and undergo a regimen of rehabilitation before discharge from the Army. This latter phase represents a different but important chapter in the handling of these cases.

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


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the rates of poliomyelitis for U.S. troops stationed abroad were higher than in the United States, and in some instances far higher (chart 3). In this chart, the rates are indicated at which poliomyelitis appeared in U.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-India theaters, and higher still in the Philippine Islands.

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

Unexpectedly, therefore, this military experience has added a good deal of knowledge to the epidemiology of poliomyelitis in general31 but relatively little to other aspects of this disease. This was because of the small 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 and Smadel in another volume in the history of the Medical Department in World War II.32 From their review, it appears that lymphocytic choriomeningitis, which had been a popular diagnosis during the late 1930's,

31(1) Paul, J. R.: Poliomyelitis in Japan. Am. J. Hyg. 45: 206-218, March 1947. (2) Sabin, A. B.: Epidemiology of Poliomyelitis; 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 Transmitted Through Contact or By Unknown Means. Washington: U.S. Government Printing Office, 1960, pp. 363-366.


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

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

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

The problem of differential diagnosis on clinical grounds in cases of aseptic meningitis was in the early 1940's, and still is, very appreciable, particularly as the list of diseases which were considered in differentiating LCM from lymphocytic meningitis in military personnel was long. It included mumps meningoencephalitis, nonparalytic poliomyelitis, central nervous system syphilis, tuberculous meningitis, acute encephalitis of a variety of causes, tetanus, brain abscess, rabies, lymphocytic meningitis associated with malaria, and infectious mononucleosis. At that time, the syndrome associated with infections by a number of Coxsackie and Echo viruses was not known, and it is highly probable that such cases were also included under the term "acute benign lymphocytic meningitis." Furthermore, the syndrome of acute, benign lymphocytic meningitis encountered in leptospirosis was also not appreciated, and it is reasonable to suppose that such cases occurred because of their subsequent detection in areas where troops were stationed during World War II.33

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

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


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special type of laboratory determinations performed, such as the serological diagnostic methods described in Circular Letters Nos. 107 and 74, and TB MED 212.

Nevertheless, it was gradually brought home to medical officers, in this country at least, that here was a disease of which, if loosely diagnosed, one could find many examples, but if rigidly diagnosed, particularly with the use of the complement fixation test, 90 percent of the cases could be eliminated. The fact that these tests were more readily available to physicians in the Medical Department of the Army than to many physicians in civilian practice indicates that here was a situation with certain educational potentialities.

In retrospect, therefore, it would seem that LCM did not prove to be a disease of military importance in World War II. The number of proved cases were few and scattered and, apparently, there was nothing special or consistent about the circumstances under which they occurred. One noteworthy feature about LCM during World War II was, however, that through the laboratories of the Army Medical Department Professional Service Schools, Army Medical Center, Washington, D.C., and a few other special laboratories, this proved to be one of the first of the virus diseases of the central nervous system in which an exact etiological diagnosis could be established by serological methods. Others in the group soon followed.

RABIES

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

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

In the three case reports reviewed, there were no special features with regard to the history, clinical course, and treatment. The incubation period in two of the patients, one of whom received a full course of antirabic inoculation, was from 3 to 6 months; whereas, in the third patient, who was bitten on the lip and who had received but three injections of vaccine, it was about 5 weeks. Once symptoms started, the course was rapidly downhill with death in 3 to 4 days. Initial symptoms included malaise, anxiety, and drowsiness. These were soon followed by nausea, pain in the shoulders, increasing stupor, rapidly developing flaccid paralysis, and pharyngeal and


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laryngeal spasm. Paraldehyde and Avertin (tribromolthanol) were employed as sedatives.

Despite the farflung activities of the U.S. Army during the course of the war, the only areas other than the United States in which the disease was contracted were, as just mentioned, Panama, the Philippine Islands, and Italy. This is extraordinary from the standpoint of the exposure which might have existed in North Africa and in the Middle East generally, but is of course not remarkable 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 American physicians to be able to look with complete equanimity on the occurrence of a dogbite. Rabies had been so long absent from Great Britain by reason of the stringent quarantine practiced in that country that no need existed for administration of antirabic vaccine after bites by dogs or other animals. The last rabies in Great Britain occurred at the time of World War I.

The rabies situation in France was almost as favorable, for apparently no definite cases of rabies had been detected in animals for some years, and no human had died from rabies in France for 16 years.

Rabies was, however, reported in Berlin, Germany, in 1945, and occasional infections among animals were recognized in northwestern European countries. Most American medical officers consequently returned to traditional practice in the 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. This bat-transmitted disease is the cause of paralysis in livestock, principally cattle. It made its first appearance in Trinidad, in 1925, where, for 11 years thereafter, focal outbreaks reoccurred in cattle, with about 1,000 cases occurring annually. The rigorous control measures which were brought to bear in Trinidad and Venezuela are described by Maj. Richard T. Gilyard, VC.35

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

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