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Chapter IV




Joseph M. Hayman, Jr., M.D.

Filariasis became a problem of importance in American or other military forces for the first time in history during World War II. In fact, the epidemic occurrence of the disease in the American military forces apparently represents the first such to be reported in medical literature, although, of course, its endemic presence in certain areas was well known. There were two principal reasons for these epidemics and for the importance which they assumed in the military and the logistic planning. These were the assignment of previously unexposed troops to endemic areas without adequate protection and the ignorance of the majority of medical officers of the early symptoms, the diagnosis, and the course of the disease.


Filariasis, contrary to common opinion, has not been unknown in the United States. The first demonstrated cases of filariasis indigenous in the United States were reported by John Guitéras in 1886.1 Though sporadic cases were reported from time to time from Florida, Alabama, and Virginia, the region around Charleston, S.C., was the only known focus of any consequence in the United States. In 1915, Johnson reported finding microfilariae in 19 percent of 400 hospital admissions within a year.2 By 1940, however, filariasis indigenous in the United States had practically disappeared, even from Charleston. This disease was probably brought to the West Indies and the Americas with the importation of African slaves.3 The absence of the disease on the Pacific coast, even in tropical America, in contrast to its wide geographic range on the Atlantic coast, supports this view, as does the fact that there is no mention of so striking a condition as elephantiasis in the early accounts of the Barbados where later it was so common that it was known as "Barbados leg." The vast majority of medical officers had no knowledge of the early symptoms or manifestations of filariasis, and their only concept of the infection was that of incapacitating elephantiasis, relatively rare even in endemic foci. The symptoms and course of filariasis in an endemic area, where exposure begins in childhood, are very different

1Guitéras, J.: The Filaria Sanguinis-Hominis in the United States. M. News (Philadelphia) 48: 399, 1886.
2Johnson, F. B.: Filarial Infection. South. M.J. 8: 630, 1915.
3Smith, A. J.: Filariasis in the Americas. In Proceedings of Second Pan American Scientific Congress, 1917, vol. 9, sec. 8, pt. 1, pp. 49-76.


from the manifestations of early infection in previously nonexposed adults. Medical literature contains only meager descriptions of the latter, and American medical officers had practically no knowledge of this aspect of the disease.


Filariasis is the term applied to infection of man and animals by certain nematodes (round worms) of the superfamily Filarioidea. Only one genus, Wuchereria, was of any military importance. This genus contains two closely related species, Wuchereria bancrofti and Wuchereria malayi. The latter is endemic in Malaya and is present in many of the islands in the Far East, as well as in parts of China and India. Few infections with this parasite were recognized in troops. Wuchereria malayi has the same life history as W. bancrofti but is believed to produce milder symptoms and not to lead to the development of elephantiasis. It will not be considered separately from W. bancrofti in this chapter.


The adult W. bancrofti are white hairlike translucent worms measuring from 25 to 100 mm. in length and about 0.01 mm. in breadth. Adult male and female worms live coiled together in the dilated lymphatics, mainly in those of the pelvic region. Occasionally, adult worms, including gravid females, are found in peripheral lymphatics and lymph nodes. The gravid female discharges sheathed embryos, periodically, which reach the bloodstream and circulate there. There is no evidence that the embryos themselves produce any symptoms. These microfilarial embryos measure about 360 by 7 microns, including sheath. The microfilariae do not develop further nor multiply in the bloodstream. Further development occurs only in the intermediate host, the mosquito. When a suitable mosquito feeds on a person with microfilariae in the peripheral blood, the embryos are taken in and enter the stomach. Here, the embryos escape from their sheaths and enter the thoracic muscles of the mosquito. In the thoracic muscles, fuller development, including one or more molts, takes place. After 10 or more days, the infective microfilariae or filariform larvae, now measuring from 1.5 to 2 mm. in length, migrate to the proboscis. When the mosquito next feeds on a person, the larvae escape and enter through the puncture wound made by the mosquito, or through abrasions in the skin, and find their way into the peripheral lymphatics and thence into the systemic circulation. It should be noted that there is no multiplication of the larvae in the insect; the larvae taken in at the time of feeding simply grow and mature into the infective stage. The time from the entry of the mature larvae to the appear-


ance of microfilariae in the blood of the host is usually stated to be about 1 year.

In most endemic areas, the microfilariae exhibit a nocturnal periodicity; that is, they are present in the peripheral blood in much greater numbers during the night than during the day, reaching a maximum between 2100 and 0200 hours. This is not true of filariasis in Samoa, Fiji, and some other Pacific islands. The reasons for this nocturnal periodicity are not known.


Filariasis is endemic throughout most of the moist and warm regions of the world between latitudes 30° N. and 32° S. In Europe, it is apparently confined to Spain (Barcelona), Hungary, and Turkey. It is present along the southern shore of the Mediterranean and is common throughout the whole central tropical belt of Africa. In the Far East, it extends along the coast of India, through Malaya, French Indochina, southern China, Korea and Japan, the Philippines, and Borneo. It is sparsely present in northern Australia. In the western world, it is common along the eastern coast of Central and South America from about central Mexico to Argentina, although it has not been reported from the west coast. It is common in the Greater and Lesser Antilles. It was formerly present in the neighborhood of Charleston (p. 123). It is endemic in the population of all major island groups in the Pacific Ocean from a latitude which would bisect the islands of Japan to one that would cross Australia just south of Brisbane, with the exception of New Zealand and the Hawaiian Islands. Throughout this filarial belt, the prevalence of the disease is spotty, large variations in incidence often being noted in adjacent villages, and is related to the flight range of the local vector.


Epidemic filariasis occurred only in troops in the South and Central Pacific Islands where microfilariae among the natives were "non-periodic" (diurnal), where the vector was an Aedes species day-biting mosquito which was present in considerable numbers, and where there was intimate intermingling of infected natives and of troops. In contrast, filariasis occurred only sporadically in other Pacific islands, such as the New Hebrides, Solomons, and New Guinea where the parasite is nocturnal. Maj. James I. Knott, MC, who was assigned to investigate filariasis in the Pacific area in March 1944,4 indicated, in his series of reports,5 that the islands where American troops had been infected were Tongareva (Penryhn), Bora-Bora

4Memorandum, Maj. O. R. McCoy, MC, Tropical Disease Control Division, to Chief, Personnel Service, The Surgeon General's Office, 21 Feb. 1944, subject: Assignment of Medical Officer for Filariasis Study.
5Reports on Filariasis Bancrofti in American Forces in the Pacific Area, April l944-January 1945, by Maj. James I. Knott, MC.


(Society), Aitutaki (Cook), Wallis, Tutuila (American Samoa), Upolu (British Samoa), Tongatabu (Tonga), and Fiji. He believed that reports of infection from Apamama (Gilberts), the Solomons, Bismarck, and New Guinea were doubtful and probably in error.

Throughout the filarial belt, some 50 species of mosquitoes, including species of Aedes, Anopheles, Culex, and Mansonia, have been reported as possible vectors. About half are known to transmit the disease naturally, while the others have been shown experimentally to permit the development of the parasite and hence are potential vectors. The majority are more active night biters, and, therefore, the disease is probably transmitted chiefly at night. But in some areas, such as Samoa,6 the principal vector is a day biter, Aedes scutellaris var. pseudoscutellaris. This one factor was probably as much responsible as any other for the large number of cases in the Samoan Defense Area. The troops in this area were instructed in preventive measures and were provided with means to prevent contact with night biters, but the importance of day feeders was not known. It should be noted, however, that many night biters will actively feed during dark days, in the jungle and in quarters.


Symptoms and Signs in Natives

To appreciate the problem presented by the epidemics of filariasis in the Armed Forces, it is necessary to point out the difference in the manifestation and course of the disease among natives in an endemic area and among adults heavily exposed for the first time. In an endemic area, children begin to be infected in infancy and presumably develop a certain degree of immunity. Iyengar7 found that the incidence of microfilariae in the peripheral blood increased from childhood up to the age of 20, and then remained constant, while the incidence of filarial disease, as manifested by symptoms, increased steadily up to the age of 45. That is, microfilariae were less apt to be found in the blood of those showing symptoms than in those symptom free. A similar decrease in the presence of microfilariae with age was found in Puerto Rico, by Bercovitz and Shwachman,8 where 5.03 percent of men between 18 and 20 years of age, but only 0.92 percent of men between 36 and 38 years of age, were positive. Of 460 men showing microfilariae in their blood, only 11 gave any history suggestive of filarial disease. Thus, in endemic areas, it appears that only a few of those infected develop symptoms, and then after some years of microfilaremia.

6Byrd, E. E., St. Amant, L. S., and Bromberg, L.: Studies on Filariasis in the Samoan Area. U.S. Nav. M. Bull. 44: 1-20, January 1945.
7Iyengar, M. O. T.: Studies on the Epidemiology of Filariasis in Tranvancore. Indian Medical Research Memoir No. 30, Supplemental Series to Indian J. M. Research, 1938.
8Professional History of Internal Medicine in World War II, The Antilles Department, pp. 131-135. [Official record.]


In a certain number of infected persons, symptoms due to obstruction of lymphatics by adult worms develop. These early symptoms-often called those of the acute stage-consist of recurring lymphangitis, adenitis, and scrotal swelling often accompanied by fever and lasting from several days to 2 weeks. Gradually, the attacks become less severe and come at longer intervals. These bouts are called elephantoid fever in some places; agua, in Barbados; mumu, in Samoa; and wanganga, in Fiji. Secondary bacterial, streptococcal or staphylococcal, infection or trauma has been held necessary for the development of these attacks. However, O'Connor,9 in 1933, showed that the presence of bacteria is not necessary for the occurrence of most of the pathological and all of the inflammatory attacks associated with filariasis. This conclusion has been amply verified by Wartman10 and by others11 from the study of cases among the Armed Forces. The role of possible toxic secretions from adult worms (uterine fluid), of products from disintegrated microfilariae caught and destroyed in lymph nodes, or of an allergic reaction in the production of these recurrent attacks has not been determined.

After the first few attacks of lymphangitis and adenitis, or of funiculitis and scrotal swelling, the limb or genitalia may return to its previous size. But, in continually reinfected natives, increasing lymphatic obstruction takes place, so that in the course of time each attack leaves a slight permanent increase in the size of the limb. "At first there is ordinary pitting edema, then swelling becomes harder and does not pit; later the whole limb becomes massive, 'brawny,' harsh and dry, the folds and cracks appear; finally these become infected with septic organisms and ulceration occurs."12 This is filarial elephantiasis, which develops most commonly in the arms, the forearms, the legs, the feet, and the scrotum. Manson-Bahr13 has pointed out that it must not be thought that lymphatic elephantiasis is solely due to filarial infection. Lymphatic elephantiasis may be congenital or familial (Milroy's or Meige's disease); it may be the result of streptococcic infection, secondary to venous thrombosis; or it may be due to obstruction from tuberculous glands or malignant growths. Other manifestations of the chronic stage of filariasis are lymph varices (most common in the groin), lymph scrotum, chyluria, chylous ascites, arthritis, and filarial abscess. These conditions are seen almost exclusively in natives of endemic areas or in persons who have lived for many years in such areas and have had repeated reinfections.

9O'Connor, F. W., cited by Lane, C.: Mechanical Basis of Periodicity in Wuchereria bancrofti Infection. Lancet 2: 399-404, 19 Aug. 1933.
10Wartman, W. B.: Lesions of Lymphatic System in Early Filariasis. Am. J. Trop, Med. 24: 299-313, September 1944.
11(1) Dickson, J. G., Huntington, R. W., Jr., and Eichold, S.: Filariasis in Defense Force, Samoan Group; Preliminary Report. U.S. Nav. M. Bull. 41: 1240-1251, September 1943. (2) Zuckerman, S. S., and Hibbard, J. S.: Clinicopathologic Study of Early Filariasis. With Lymph Node Biopsies. U.S. Nav. M. Bull. 44: 27-36, January 1945.
12Napier, L. Everard: The Principles and Practice of Tropical Medicine. New York: The MacMillan Co., 1946,  p. 674.
13Mason-Bahr, Philip H.: Tropical Diseases, 11th edition. Baltimore: Williams & Wilkins Co., 1942, p. 759.


Symptoms and Signs in Military Personnel

The picture of filariasis as it occurred in the Armed Forces was quite different. Symptoms usually began to appear from 5 to 18 months after first possible exposure and consisted of pain, swelling, or redness of an arm or a leg, or pain and swelling in the scrotal region. Constitutional symptoms, such as chills, fever, malaise, or headache, were rarely reported. A few cases developed symptoms as early as 3 months after the first possible exposure.14 In this regard, the case of O'Connor's assistant who developed epitrochlear adenitis 43 days after being bitten by a filariated mosquito is pertinent.15 Dickson, Huntington, and Eichold16 described a case in which adult worms were recovered 5½ months after the first possible exposure to filariasis.

The observations on different groups of infected men were described in a number of reports to The Surgeon General and later published in the literature. These have been reviewed by Wartman17 who gives an extensive bibliography. Many men were only exposed in an endemic area for 1 to 2 months, so that symptoms did not develop until their removal to a non-endemic area. In other groups, symptoms began to develop while the troops were still in the endemic area. No relation was noted between season and onset of symptoms, nor to time of day.

When the reports of different observers are combined, symptoms referable to the genitalia were the most common initial complaint, although varying from 1118 to 97 percent19 in different reports. The commonest complaint was of heaviness or mild pain in the scrotum, less often in the groin, frequently first noticed after severe exertion and usually made worse by exercise. On examination, edema of the spermatic cord was the most constant finding.20 This might be present alone; however, it was frequently accompanied by the swelling of the epididymis or the testicle and by the presence of a hydrocele or scrotal edema. Absence of the cremasteric reflex on the affected side, attributed to edema of the cremasteric muscle, was thought a helpful early diagnostic sign in some cases.21 The left spermatic

14(1) King, B. G.: Early Filariasis Diagnosis and Clinical Findings; Report of 268 Cases in American Troops. Am. J. Trop. Med. 24: 285-298, September 1944. (2) Burhans, R. A., Camp, J. D., Butt, H. R., and Cragg, R. W.: Lymphangitis of Suspected Filarial Origin; Preliminary Report Concerning Its Treatment. U.S. Nav. M. Bull. 42: 336-340, February 1944.
15O'Connor, F. W., and Hulse, C. R.: Some Pathological Changes Associated With Wuchereria [Filaria] bancrofti Infection. Tr. Roy. Soc. Trop. Med. & Hyg. 25: 445-454, May 1932.
16See footnote 11 (1), p. 127.
17Wartman, W. B.: Filariasis in American Armed Forces in World War II. Medicine 26; 333-394, December 1947.
18Smith, F. R., Jr.: Filariasis; Study of 737 Patients So Diagnosed. U.S. Nav. M. Bull. 44: 719-725, April 1945.
19Johnson, P. A. G.: Filariasis; Clinical Findings in 189 Cases. U.S. Nav. M. Bull. 43: 950-954, November 1944.
20Hodge, I. G., Denhoff, E., and Vander Veer, J. B.: Early Filariasis (Bancrofti) in American Soldiers. Am. J.M. Sc. 210: 207-223, August 1945.
21Saphir, W.: Filariasis; Early Clinical Manifestations; Analysis of 35 Cases. J.A.M.A. 128: 1142-1144, 18 Aug. 1945.


cord was involved more frequently than the right. Bilateral involvement was not uncommon.

The entire cord from the internal ring to its junction with the epididymis might be involved. In some cases, there was only slight thickening of one side as compared with the other, or the entire cord would be enlarged from two to five times its normal size. The swollen cord was usually rubbery in consistency, but sometimes nodular. The pain varied from slight discomfort to exquisite pain, similar to that resulting from a blow to the scrotum. The funiculitis was descending or retrograde, similar to the lymphangitis seen in the extremities. Fogel and Huntington22 were able to follow the development of the lesion in three hospital corpsmen. The onset consisted of lower abdominal pain at which time the spermatic cords were normal on palpation. The authors noted, as follows:

Within 12 hours there was palpable swelling high up in the inguinal canal. The examining finger could be inserted through the external inguinal ring without causing much discomfort to the patient. As the hours passed the progress of the swelling could be palpated as it moved down the cord. Within 24 hours that part of the cord lying within the inguinal canal was greatly swollen and tender. It was difficult to pass the palpating finger through the external ring because of the swelling and tenderness of the cord. In the succeeding 24 hours a scrotal mass was visible and palpable.

Such observations leave little doubt that the acute funiculitis was an acute lymphangitis of the spermatic cord. As with other filarial lesions, the swelling of the cord subsided in a few days to 2 weeks, often to recur one or more times at varying intervals. Frequently, especially after several attacks, slight painless enlargement of the cord persisted and was probably the most permanent of all physical findings.23

According to King,24 the globus major was most frequently involved, and the body and globus minor only infrequently. In most instances, the lesion subsided completely, but in some cases thickening and palpable nodules remained. Some attached considerable significance to the presence of a small, shotlike lymph node, located where the vas deferens becomes distinctly palpable from the epididymis, which might persist for many months.

Acute orchitis, unilateral or bilateral, occurred in from 14 to 54 percent of reported cases. Symptoms consisted of pain, swelling, and tenderness. The pain might radiate up to the spermatic cord, or it might appear first in the lower quadrant of the abdomen and radiate downward to the spermatic cord and the testicle. Pain was usually not severe. Aspiration in a few cases yielded a small amount of fluid similar to that obtained from an ordinary hydrocele. Inflammation of the scrotal skin was not uncommon, usually in the most dependent portion of the scrotum, and was not related

22Fogel, R. H., and Huntington, R. W., Jr.: Genital Manifestations of Early Filariasis. U.S. Nav. M. Bull. 43: 263-270, August 1944.
23Leede, W. E., and Josey, A. I.: Early Diagnosis of Filariasis and Certain Suggestions Relative to the Cause of Symptoms. Ann. Int. Med. 23: 816-822, November 1945.
See footnote 14 (1), p. 128.


to the degree of swelling of the cord. Microfilariae were not found in aspirated hydrocele fluid. Varicocele was reported by a number of observers, usually on the left side, but its relationship to filariasis was not determined and certainly is open to serious question.25

Acute lymphangitis was the most striking and characteristic physical finding in acute filariasis, and the one most helpful in making the clinical diagnosis. It occurred in the arm, the leg, the buttock, the groin, the abdomen, or the neck. Regardless of location, retrograde spread was characteristic, often starting from a palpable lymph node. It was about twice as common in the arms as in the legs in all series reported from the Pacific islands. This is the reverse of Grace's26 report from British New Guinea where four-fifths of the patients showed involvement of the legs first. The lymphangitis of the arms occurred most commonly along the course of the brachial vessels or on the volar surface of the forearm. It took one of three forms-as a red streak of varying length, often with an underlying firm, irregular cord; as a patch of subcutaneous edema and overlying redness, irregular in outline and of varying size, most commonly occurring on the inner anterior surface of the forearm, just below the elbow; or as a diffuse edema and erythema of the upper part of the arm or the forearm. With erythema, there was local heat, but again tenderness was only mild or moderate. The red streaks were usually shorter, broader, and more diffuse than in bacterial lymphangitis. The characteristic retrograde progression, in contrast to the centripetal progression of bacterial infection, should be stressed. Lymphangitis of the extremities progressed from the axilla down the arm to the elbow, from the antecubital region down the forearm to the wrist, or from the inguinal region either down the inner aspect of the thigh or around the lateral aspect of the thigh, above the greater trochanter, to the gluteal region.

Hodge, Denhoff, and Vander Veer27 believed that involvement of the deep lymph vessels of the abdomen should be considered in the presence of pain in the flank or the abdomen, with radiation to the genitalia or the thigh, and tenderness of the abdomen on the affected side. It is obvious that other causes of these symptoms, such as appendicitis and renal, ureteral, and retroperitoneal pathological conditions, should be excluded before considering filariasis as the explanation of the symptoms. An attack of lymphangitis often began to fade in 24 hours, and lasted from a few days to 2 weeks. Recurrences were common and characteristic. Chronic lymphangitis, however, was rare.28 Persistent lymph edema was also rare.29

25See footnote 17, p. 128.
26Grace, A. W.: Tropical Lymphangitis and Abscesses. J.A.M.A. 123: 462-466, 23 Oct. 1943.
27See footnote 20, p. 128.
28Behm, A. W., and Hayman, J. M., Jr.: Course of Filariasis After Removal From Endemic Area. Am. J.M. Sc. 211: 385-394, April 1946.
29Coggeshall, L. T.: Lymphadenopathy and Filariasis. (Abstract) Bull. U.S. Army M. Dept. 5: 250, 1946.


Enlarged, slightly tender, discrete lymph nodes without attachment to the skin or without suppuration were described by all authors and constituted the commonest symptom attributable to filariasis. Most critical medical officers found it difficult to judge the significance of enlarged nodes, particularly when the enlargement was slight, nontender, and in the more common sites for palpable nodes, such as the axilla and the groin. Among marines at Klamath Falls, Ore., Coggeshall30 found enlarged nodes in 60 percent of 200 men diagnosed as filariasis, in 57 percent of 271 men evacuated for malaria, and in 50 percent of 98 controls who had never been overseas. Adenopathy was more suggestive of filariasis when the enlargement came on acutely without ascribable cause and when it occurred in places where enlarged nodes are not usually palpable, such as the antecubital area, the epitrochlear region, particularly above the site of the common epitrochlear node, the intercostal region, the popliteal space, in the back, the wrist, the tip of the ilium, or in the region of the teres and serratus muscles.

Transient or fugitive swellings, believed to be evidence of hypersensitivity to filarial products, were described in arms, legs, hands, feet, torso, eyelids, and forehead. According to Burhans, Camp, Butt, and Cragg,31 the swellings developed along the path of lymphatic vessels or at the edges of muscles. Fogel and Huntington (p. 129) observed them in areolar tissue. These swellings were raised, usually slightly tender, and sometimes resembled erythema multiforme. They lasted from a few days to 2 weeks and disappeared without residua. No worms were found in biopsies from such swellings.

Filarial abscess, or abscess or suppurating nodes attributed to filariasis, was extremely rare. Glauser32 reported three cases and Englehorn and Wellman33 two cases. No worms or filariae were found in the pus.

The initial attack lasted from 3 to 5 days to 2 weeks, occasionally as long as a month. King34 recorded fever in 53 (19.7 percent) of 268 cases. Usually, the temperature did not exceed 99° or 100° F., but in a few cases it reached 102° or 104° F. A striking feature of these attacks was the lack of severe constitutional symptoms. The patients did not feel sick, and the local lesions were not extraordinarily painful. In no instance did there seem to be danger to life. From the military standpoint, the attacks were most important because the lesions were incompatible with full field duty. The average hospital stay in King's series was 15.9 days.

Recurrences of adenopathy, lymphangitis, and scrotal swelling were common and characteristic. They occurred at intervals of a few days to

30Coggeshall, L. T.: Filariasis in Serviceman; Retrospect and Prospect. J.A.M.A. 131: 8-12, 4 May 1946.
31Burhans, R. A., Camp, J. D., Butt, H. R., and Cragg, R. W.: Lymphangitis of Suspected Filarial Origin; Preliminary Report Concerning Its Treatment. U.S. Nav. M. Bull. 42: 336-340, February 1944.
32Glauser, F.: Filariasis in Returning Marines. U.S. Nav. M. Bull. 44: 21-26, January 1945.
33Englehorn, T. D., and Wellman, W. E.: Filariasis in Soldiers on Island in South Pacific. Am. J.M. Sc. 209: 141-152, February 1945.
34 See footnote 14 (1), p. 128.


several months. Relapses became less frequent and severe with the passage of time, but during the first 12 to 18 months this was not always true, and not infrequently a relapse would be more severe than the initial attack. Relapse was observed as long as 2 years after the initial attack.35 The frequency of relapse diminished rapidly after evacuation to the United States. Complaints of subjective symptoms were far more common than objective findings. Coggeshall (p. 131) commented that men assigned to tasks they liked did not complain; men on the football and basketball teams did not experience any difficulty, while men on guard duty or police detail would complain bitterly. Behm and Hayman36 believed that complaints of pain unaccompanied by recurrence or increase in swelling of nodes, scrotal contents, or lymphangitis should not be regarded as due to filariasis but rather should be more properly interpreted as due to muscle strain, fatigue, arthritis, or some other cause. Nearly all observers believed that relapses were prone to be precipitated by severe physical exertion.37 Coggeshall, however, was unable to precipitate a recurrence by exhausting exercise in 10 marines after their return to Klamath Falls. Behm and Hayman reported from a study of 408 men, diagnosed to have filariasis, who had been in a hyperendemic area for 1 year and then observed for 14 months after removal, that the number of attacks varied from 1 to 13, as follows:

Number of attacks

Number of men















No attacks were observed in this group later than 13 months after removal from the endemic area. A number of other reports noted the rapid disappearance of signs and symptoms after return to the United States.38

Laboratory Examinations

Routine laboratory examinations were of little value in diagnosis.39 No abnormalities of the urine attributable to filariasis were described. From the reported data, the total white blood cell count averaged about 9,000, with extremes of 3,600 and 19,000 per cubic millimeter. There was no significant alteration in the number or the form of neutrophils, lymphocytes,

35Coggeshall, L. T.: Malaria and Filariasis in Returning Serviceman; Ninth Charles Franklin Craig Lecture. Am. J. Trop. Med. 25: 177-184, May 1945.
36See footnote 28, p. 130.
37(1) Brown, Maj. T. McP., Stifler, Capt. W. C., and Bethea, Capt. R. W., Jr.: Supplementary Report From the 118th General Hospital on 536 Officers and Enlisted Men From 134th Field Artillery Battalion, 31 July 1944. (2) See footnote 28, p. 130, and footnote 23, p. 129.
38(1) See footnote 32, p. 131, and footnotes 18 and 19, p. 128. (2) Zeligs, M. A.: Psychomatic Aspects of Filariasis; Present Day Evaluation, J.A.M.A. 128: 1139-1142, 18 Aug. 1945.
39See footnote 17, p. 128.


or mononuclear cells. In his review, Wartman observed: "Eosinophilia occurred in one-half to two-thirds of the cases, the average being about 850 cells per cu. mm. Most authors thought the presence of eosinophilia was not helpful in diagnosis." Eosinophilia was not observed in Leede and Josey's patients. On the other hand, King, and Hodge, Denhoff, and Vander Veer found that the incidence of eosinophilia (9 percent or above) was significantly greater in soldiers exposed to filariasis. Among exposed troops with signs of filariasis, the incidence of eosinophilia was greater than in those with no evidence of the disease but was twice as great in those with slight or doubtful findings, as in those with frank clinical filariasis. No significant changes were found in red blood cell counts, hemoglobin, or sedimentation rate. Bacterial cultures of biopsy material, blood, aspirated fluid from lymph nodes, and hydroceles showed no pathogens.

Despite many thousands of blood examinations, by all known methods, at all times of the day and night, microfilariae were only found in the blood of approximately 20 cases. Since some of these men had served in Puerto Rico, the source of infection could not always be established. Flynn40 found 8 positive blood or lymph node aspiration material in 125 patients. Hodge, Denhoff, and Vander Veer (p. 128) found a single microfilaria in 2 blood samples among over 2,000 taken from 266 soldiers. Leede and Josey found microfilariae once in an individual who had lived for years in an endemic zone in childhood. Goodman, Weinberger, Lippincott, Marble, and Wright41 reported finding microfilariae on one occasion in each of 2 soldiers among 145 examined on 7 nights and 3 days by the Knott concentration method. In other large groups of men, including those reported by King and by Behm and Hayman, no microfilariae were found despite careful and repeated study by Knott's method as well as by thick smears.

The "new" disease which was epidemic among troops in certain Pacific areas was first definitely established as filariasis by the demonstration of adult worms and microfilariae in biopsied lymph nodes and lymphatics. Wartman (p. 127), Michael,42 Hartz,43 and Rifkin and Thompson44 described the pathological findings in biopsy material, and Wartman (p. 128) summarized all the material available in the Army Institute of Pathology. As a result of these studies, Wartman concluded that it was clear that the adult filaria worms in the lymphatic system might cause a granulomatous inflammatory reaction. When in lymph nodes, the changes were often not confined to the immediate vicinity of the worms but were present throughout

40Flynn, P. D.: Filariasis Suspects; Review of Cases Admitted. U.S. Nav. M. Bull. 42: 1075-1079, May 1944.
41Goodman, A. A., Weinberger, E. M., Lippincott, S. W., Marble, A., and Wright, H. W.: Studies of Filariasis in Soldiers Evacuated From South Pacific. Ann. Int. Med. 23: 823-836, November 1945.
42Michael, P.: Filariasis: Histopathologic Study. U.S. Nav. M. Bull. 45: 225-236, August 1945.
43Hartz, P. H.: Contribution to Histopathology of Filariasis. Am. J. Clin. Path. 14: 34-43, January 1944.
44Rifkin, H., and Thompson, K. J.: Structural Changes in Early Filariasis. Arch. Path. 40: 220-224, October 1945.


the node. Michael believed that the sex of the infecting worm influenced the histological changes, male worms degenerating somewhat earlier and faster than females, and fertilized females still more slowly. Many of the changes found in worm-infested nodes were also observed in tissues in which no parasites were discovered, even in serial sections. Biopsies of such nodes at the height of enlargement showed marked hyperplasia, infiltration with eosinophils, and distention of lymphatic sinuses. Changes in lymph vessels consisted of dilatation, lymph thrombosis, and acute lymphangitis which was sometimes necrotizing. In some, these changes appeared reversible, but in others fibrosis and obstruction of the affected lymphatic vessel had ensued. No difference could be detected in the changes associated with the presence of living or dead worms. From his failure to find parasites in genital lesions, Michael speculated that many genital enlargements were toxic or allergic in nature, and not due to direct invasion of the organs by parasites, and that therefore the changes could be presumed to be reversible. In a study of 58 biopsies from the Pacific area, Wartman found adult worms in 8 (13.8 percent) and microfilariae in 3 (5.1 percent) and regarded the histological picture in 24 (51.0 percent) of the biopsies that showed no parasites as characteristic of the disease. Michael reported finding adult worms in 30 percent of 120 biopsies. He also pointed out that, if a cut node is placed in saline solution, the adult worm may be found in the ambient fluid in 24 to 48 hours, thus saving the labor of serial sections. While the demonstration of adult worms or microfilariae is satisfactory proof of the diagnosis, biopsies should not be undertaken lightly or routinely. Biopsies from the inguinal and femoral region are usually unsatisfactory and frequently lead to prolonged disability. Excision of lymph nodes or other tissue while acute symptoms are present may be followed by severe exacerbation of symptoms. An epitrochlear or other unusually enlarged node, or a palpable lymphatic cord, taken as an attack subsides is apparently the most profitable site for biopsy.

Because of the failure to demonstrate microfilariae in the blood and the difficulty in making a reasonable clinical diagnosis of filariasis, numerous attempts were made to develop a satisfactory laboratory test. Older observations had shown that there is in the filariids a common group reacting factor capable of eliciting an intradermal response in persons harboring filarial infection and that antigens prepared from these filariids could also be used in serologic tests. Because of the impracticality of obtaining adult W. bancrofti, most workers had used a related filariid, especially the dog heartworm, Dirofilaria immitis. Taliaferro and Hoffman45 had originally used a 1: 200 dilution of saline extract of the dog heartworm, while Fairley46 found that a 1: 1,000 dilution gave fewer false positive reactions.

45Taliaferro, W. H., and Hoffman, W. A.: Skin Reactions to Dirofilaria immitis in Persons Infected With Wuchereria bancrofti. J. Prev. Med. 4: 261-280, July 1930.
46Fairley, N. H.: The Skin Test and Complement Fixation Reaction in Filariasis. Tr. Roy. Soc. Trop. Med. & Hyg. 25: 220, 1932.


Since no prepared antigen was available from supply, oversea units prepared their own antigens from D. immitis procured locally. King47 showed that even minor differences in the method of preparation made significant differences not only in patients but in controls. The results of these studies, both overseas and in the United States, are summarized by Wartman. In general, antigens prepared from D. immitis gave false positive reactions in 5 to 14 percent of men who had never been in an endemic area and in 83 to 91 percent of those showing clinical symptoms that might be filariasis. A finding that made the interpretation of these skin tests particularly difficult was the increased incidence of positive reactions in men who had tropical service in a nonfilarial area or in one of very low endemicity, as well as among those who had served in an endemic area but had never had symptoms. The former was as high as 27 percent in some series. The latter might be attributed to a "biological" rather than a "clinical" infection; that is, to an infection sufficient to produce skin sensitization but no symptoms, comparable to that observed in certain individuals who give a positive reaction to Trichinella antigen. Huntington's48 conclusions that while the skin test is helpful in the general study of the incidence and epidemiology of filariasis, it is not particularly helpful in the diagnosis of individual cases, would be echoed by most observers. Both immediate and delayed reactions were observed; the immediate being apparently the more sensitive, the delayed giving fewer false positive reactions. The use of other filariid antigens (Setaria equina, Litomosoides carinii) gave similar results. The presence of intestinal helminths apparently made no significant difference in the incidence of positive reactions. Bozicevich and Hutter49 believed that the test was made more specific by use of a 1: 8,000 dilution of antigen. Complement fixation and precipitin reactions were not found to be particularly useful.

With this brief review of filariasis, as described in most textbooks of medicine, and of the symptoms and findings in acute epidemic filariasis as encountered among military personnel in World War II, it is hoped that the description of the experience in different units (p. 138) and in the various theaters can be appreciated.


When the marines went into the Samoan area early in 1942, there was extreme military necessity of getting under cover as quickly as possible. The native villages were the most available sites. As a result, there was intimate contact between troops and the heavily infected native population.

47See footnote 14 (1), p. 128.
48Huntington, R. W., .Jr.: Skin Reactions to Dirofilaria immitis Extract. U.S. Nav. M. Bull. 44: 707-717, April 1945.
49Bozicevich, J., and Hutter, A. M.: Intradermal and Serological Tests With Dirofilaria immitis Antigen in Cases of Human Filariasis. Am. J. Trop. Med. 24: 203-208, May 1944.


The possibility that the troops might become infected with filariasis was not seriously considered, for the region had been occupied by white men for a number of years without evidence of infection. Indeed, some believed that the white man was not susceptible. Previous white residents of the area had lived apart from native villages and in screened quarters. Moreover, while the men were equipped with mosquito nets, it was not recognized that the important vector of filariasis in this area was the day-biting A. scutellaris var. pseudoscutellaris and that the microfilariae in this area were nonperiodic. As a consequence of living in and near native villages and of a day-biting vector, these men were subjected to a large number of infected bites in a relatively short time. In all of the Pacific islands, a high incidence of infection among troops occurred only where these two conditions existed.

It is difficult to get precise data on the number of men infected. Coggeshall (p. 131) estimated that 38,300 men of the U.S. Navy and the U.S. Marine Corps were exposed, and a filarial registry showed 10,421 diagnosed cases. Many of these were erroneous diagnoses, but on the other hand there were many cases in which the diagnosis of filariasis was not entered on the health record.

The approximate number of primary admissions for filariasis in the years 1942-45 is shown in table 18. One death was recorded in an oversea theater in 1944.

TABLE 18.-Admissions for filariasis in the U.S. Army, by area and year, 1942-45


Number of cases






Continental United States



























Middle East














Southwest Pacific







Central and South Pacific







North America2







Latin America






Total overseas






Total Army






1Includes North Africa.
2Includes Alaska and Iceland.
3Includes admissions on transports.


The admissions tabulated as from continental United States represent infections acquired overseas. The marked decrease in 1945 as compared with 1944 was due to the movement of the war away from hyperendemic areas, as well as to better mosquito control, and to the separation of troops and natives. The average number of days lost per man in 1943 was 112, while in 1945 it was 66. The annual admission rate for filariasis per 1,000 mean strength in the Central and South Pacific Area was 1.91 in 1943 and 1.69 in 1944. A few cases were reported in Puerto Rican troops who had probably been infected in Puerto Rico before military service. The chief sources of infection in Army units were Bora Bora, Aitutaki, Tongareva, Fiji, and Tongatabu Islands (pp. 125-126).


Full consideration must be given to the fact that the military activities in the Pacific areas early in the war were such that the tactical situation had highest priority. In commenting on the epidemic in Samoa, Wallis, and Aitutaki, Knott reported50 that recommendations by medical officers that natives be removed from camp areas raised objections from island governments and were vetoed by area commanders. Many medical officers could not believe that the lymphangitis observed in troops was filarial. No one was to speak or write of filariasis. To combat rumors, Knott reported, the area commander put out the famous order that no case was to be called filariasis because "this disease does not affect white men." The men themselves, however, believed the natives. Shortly after this order, the diagnosis was settled by finding worms in biopsy material. Knott commented further:

The army units in the Central Pacific Area were not warned officially that filariasis had broken out in the marines on Samoa and Wallis when it first broke out, but the medical officers promptly passed the word along to the others. Officers from the Army islands visited Samoa and learned what they could. But here again the information was gotten after the units had already been infected. And again, the medical officers could not convince the island commanders that they should exclude the natives from the camp areas. Perhaps the area commanders would have listened to the medical officers if they had had scientific data to prove the danger of the situation. But there were no epidemiologic mosquito survey, nor mosquito control units in the area.

The men who had seen examples of filariasis among the natives were extremely fearful of the diagnosis, believing that they would suffer similar disfigurement and particularly that they would be sterile. The obvious ignorance of medical officers of the disease only seemed to increase this apprehension, lower morale, and lead to the conviction of the men that they had been afflicted with a serious and incurable disease about which nobody knew anything. Examples of the ignorance of the disease are the remark of a (Navy) consultant who when shown sections of worms in biopsied glands said that this couldn't be filariasis, since no microfilariae were found in

50See footnote 5, p. 125.


peripheral blood but must be a new disease,51 and by the action of a post medical inspector who, in recording the admission of 108 patients diagnosed filariasis, reported as follows:

Immediate and rigid precautions were taken to isolate patients by restriction of the patients to the ward several hours before dusk; by careful, complete screening of the building in which they were housed; by spraying of the screens and doors several times during the day and night. * * * blood smears were taken during day and night in an attempt to detect the presence of microfilariae. However, these smears were entirely negative.52

The impact of such treatment on the emotional reaction of the men and their families can well be imagined.

Another example of ignorance of the disease was noted in a report53 which contained the following statement:

It is known that the microfilaria cannot reproduce themselves asexually. It takes a number of months for the microfilaria to develop into the adult macrofilaria. We have seen adult macrofilaria in the human from 15 to 18 months after exposure and so know that the adult forms can develop in this time; * * *. It is necessary to have an adult male and female macrofilaria in close harmony to produce sexually mature microfilaria.

It is hard to believe that the writer, who was making the diagnosis of filariasis and talking to patients, knew even the life cycle of the parasite!

That the disease was filariasis was recognized officially in a directive from the Surgeon General of the Navy, dated 23 May 1943. The directive clarified the administrative handling of filariasis and directed that those so diagnosed be transferred to the nearest U.S. naval hospital in the United States to be hospitalized until free from symptoms and not to be sent again into endemic areas. The presence of microfilariae did not restrict movement. No such definite evacuation policy was established by the Army.54 War Department Circular No. 189, 21 August 1943, specified that filariasis was disqualifying for service in tropical areas; War Department Circular No. 293, 11 November 1943, provided that men suffering from filariasis would not be dispatched overseas; and War Department Technical Bulletin (TB MED) 142, "Filariasis (Wuchereria) With Special Reference to Early Stages," appeared in February 1945, but by this time the epidemic overseas was past.


The history of two Army units illustrates the difficulty in diagnosis, the results of indecision, and the loss in manpower caused by filariasis. The 134th Field Artillery Battalion and the 404th Combat Engineer Company (Separate) were dispatched overseas in April 1942 and were stationed

51Personal experience.-J. M. H., Jr.
52Monthly Sanitary Report for Month of July, Halloran General Hospital, 3 Aug. 1943.
53Essential Technical Medical Data, South Pacific Base Command, for February 1945, dated 12 Mar. 1945.
54To the best of my knowledge.-J. M. H., Jr.


on Tongatabu, where the nonperiodic form of filariasis was highly endemic, from May 1942 to May 1943. No symptoms recognized as due to filariasis developed during this time. These units left Tongatabu in May 1943, stopped at New Caledonia and in Townsville, Australia, and then were stationed on Woodlark Island, southeast of New Guinea, until January 1944. While Woodlark Island is in the filarial zone, the endemicity is extremely low, if any. An Australian mine superintendent who had lived on the island for 30 years reported that he had never seen evidence of the disease among natives, and physical examinations and blood smears on 100 natives showed no evidence of filariasis.55 In addition to the men who had been on Tongatabu, 145 replacements were with them on Woodlark. Recurrent lymphangitis, scrotal swelling, and adenopathy began to develop in the Tonga group about August 1943. Many men who complained of pain and discomfort showed no significant physical findings. Similar symptoms developed at the same time among the replacements who had never been on Tongatabu. Because of the number of men exhibiting symptoms, the uncertainty of the actual number infected, and the loss of morale and efficiency, the units were transferred to Sydney, Australia, and examined by the staff of the 118th General Hospital.56 In addition to history, physical examination, and blood studies, skin tests were done with a 1:1,000 extract of D. immitis. The results of these skin tests are shown in table 19.

TABLE 19.-Results of skin tests for filariasis, 118th General Hospital, 1944

Group tested

Number of tests

Positive reaction















No tropical service




1Personnel of 118th General Hospital.

On the basis of history, examination, and skin tests, it was concluded that 494 of 526 men who had been on Tonga and 17 of the 144 who had only been on Woodlark showed evidence of filariasis. The commanding officer of the Sixth U.S. Army recommended that these units be returned to the United States because (1) their combat efficiency had been seriously impaired, (2) rehabilitation would extend over a long period, (3) their future combat value was highly doubtful, and (4) replacement of all individuals

55Letter, Maj. Albert M. Dashiell, Headquarters, Sixth Army, to Surgeon, Sixth U.S. Army, 11 Nov. 1943, subject: Filariasis.
56Brown, Maj. T. McP., Stifler, Capt. W. C., Jr., and Bethea, Capt. W. R., Jr.: Preliminary Report of Filariasis Survey of 501 Men From 134th Field Artillery Battalion and 171 Men From 404th Combat Engineer Company (S), 10 Mar. 1944.


showing evidence of filariasis would result in a state of training far below that required for efficient combat.57

The personnel of the organizations returned to the United States as patients in July 1944. When they reached Moore General Hospital, Swannanoa, N.C., the troops had been overseas 27 months, had never been in combat, and had been hospitalized for 7 months. The men were confused, apprehensive, and discouraged. They had, many of them, seen some of the late sequelae of filariasis, had been conscious of the concern and indecision of the medical officers who had examined them, and commonly believed that they were afflicted with an incurable, progressive, and eventually disfiguring and incapacitating disease. This was borne out by the men's own opinion of their ability to do duty. Of the 134th Field Artillery who had been on Tonga, 24 percent thought they were fit for full duty, 70 percent that they were fit only for limited duty, and 6 percent that they were completely incapacitated. After thorough study and from 2 to 10 months' observation, 196 (36.8 percent) of those who had been on Tonga were diagnosed as filariasis. Of these, three were separated from the service because of filariasis, one with persistent lymph edema of both legs, one with a lymph scrotum, and one with recurrent lymphangitis; the others were returned to duty in the Zone of Interior in accordance with current directives. No microfilariae were demonstrated on repeated search. The number of recurrent attacks of lymphangitis, adenopathy, or scrotal swelling was difficult to estimate, since many more were recounted by the men than were documented in medical records or observed by a medical officer. On the basis of histories of 408 men, 139 stated that they had had a single attack; 99, two attacks; 76, three; 53, four; 10, six; and only 10, more than 10 recurrences. No evidence of recurrence of physical findings that could be attributed to filariasis was observed later than 25 months after removal from the endemic area. Of 308 men returned to duty as nonfilarial and followed for an additional 8 months, 3 presented sufficiently characteristic symptoms of recurrent adenopathy to justify a change in diagnosis to

TABLE 20.-Comparison of results of skin tests for filariasis, with D. immitis antigen, overseas (February-March 1944) and Zone of Interior (September 1944)

Group tested

Percent positive with antigen dilution of

(February-March 1944)

(September 1944)










57Letter, Lt. Gen. Walter Krueger, Headquarters, Sixth U.S. Army, to Commanding General, U.S. Army Forces, Far East, 8 Apr. 1944, subject: Return of 134th Field Artillery Battalion and 404th Engineer Company (C) (Separate) to the United States.


filariasis. The entire group was skin tested according to the technique of Bozicevich and Hutter, using a 1: 8,000 dilution of antigen. The results of these tests in comparison with those done overseas are shown in table 20.

Of the men discharged because of filariasis, 79.5 percent had a positive skin test while 42.0 percent of the "not filariasis" Tonga group and 19.1 percent of the Woodlark group did also. The former might be thought of as due to a "biological" rather than "clinical" infection; that is, to an infection sufficient to produce skin sensitivity but no symptoms, comparable to that observed in certain individuals who give a positive reaction to Trichinella antigen. But it is hard to apply this explanation to the Woodlark group where the possibility of infection was very problematical. This obviously makes the skin test of less value in the individual case than would be desirable.

The history of these two units has been given in some detail because they were the most carefully studied of Army units and because the experience in other groups of men exposed in hyperendemic areas was similar. The amount of physical incapacity was slight in proportion to that produced by fear, anxiety, and uncertainty. Zeligs58 presented factual data which showed that these fears were groundless. The longer the period of inactivity because of a diagnosis of filariasis, the more difficult it was to return men to duty. When presented with evidence of their ability to lead normal lives and with the demonstration that they could exercise without producing symptoms, most men ceased to be concerned. Those with a past history of psychoneurotic behavior, or where the element of secondary gain was prominent, frequently used filarial symptoms to help solve preexisting emotional problems or to escape unpleasant situations. The ignorance of most medical officers of the disease led to a diagnosis of filariasis in men who had never been in an endemic area or who suffered from angioneurotic edema, thrombophlebitis lymphogranuloma venereum, and epididymitis secondary to a urethritis.


The diagnosis of early filariasis is not easy. Demonstration of microfilariae in the peripheral blood or of adult worms in biopsy material is the only proof. Care should be taken with blood smears to prevent contamination with filarial-like structures.59 Usually, the diagnosis must be made on history and clinical findings. History of exposure in an endemic area is of prime importance; the diagnosis should not be entertained without it. History of lymphangitis, adenopathy, or scrotal pain is unreliable. An acute attack of retrograde lymphangitis, adenopathy, particularly in

58See footnote 38 (2), p. 132.
59Manson-Bahr, P.: A Spurious Blood Parasite From Fiji. Tr. Roy. Soc. Trop. Med. & Hyg. 45: 12, 1951.


unusual locations, funiculitis, epididymitis, or orchitis should be observed. All other discoverable causes for the symptoms should be excluded. The skin test is helpful in surveys but is not reliable in the individual. Exercise tests are of value where they precipitate acute attacks.60


Prevention of infection in troops depends upon information on the presence of microfilariae among natives, whether the parasite is diurnal or periodic, and on the important local vectors. The greatest danger is where the parasite is diurnal and the vector a day biter. Under such conditions, separation of troops and natives is essential. Studies by Byrd, St. Amant, and Bromberg61 showed that, while 25 percent of Aedes scutellaris collected in the center of a native village might be infected, the infection rate dropped to zero at 200 yards. Thus, while this mosquito has a short flight range, other vectors have a longer range. Where the tactical situation permits, troop areas should be at least 1 mile from native villages, or the latter moved. All methods for mosquito control should be instituted. Where the vector is a day biter, preventive measures, such as the wearing of long sleeves and full-length trousers and the frequent application of repellent, should be enforced.

The value of observing the principles of military sanitation was shown by Lt. Gen. Thomas E. Watson, U.S. Marine Corps,62 on the island of Upolu. About 90 percent of the troops were in a camp around an airfield. Natives were excluded from the camp, and mosquito-control measures were carried out in the area. Only rare cases of filariasis developed, and these may not have been acquired in the area. The other 10 percent of troops, stationed in the town of Apia, intermingled with natives and a number acquired filariasis.

When the presence of filariasis among troops was recognized, measures were taken not only to prevent further infection, but to minimize the possibility of development of late complications from prolonged exposure. Filariasis was designated as disqualifying for duty in tropical areas, and later for any oversea assignment (p. 138).

Another problem arose late in the war with the transfer of prisoners of war from heavily infected Pacific islands to Hawaii and continental United States where possible vectors existed.63 Between June 1945 and the end of hostilities, over 4,000 prisoners from Okinawa were received

60War Department Technical Bulletin (TB MED) 142, February 1945.
61See footnote 6, p. 126.
62See footnote 5, p. 125.
63(1) Newton, W. L., Wright, W. H., and Pratt, I.: Experiments to Determine Potential Mosquito Vectors of Wuchereria bancrofti in Continental United States. Am. J. Trop. Med. 25: 253-261, May 1945. (2) Scott, O. K., Richards, C. S., and Seaman, E. A.: Experimental Infection of Southern California Mosquitoes With Wuchereria bancrofti. J. Parasitol. 31: 195-197, June 1945.


in the Hawaiian Islands, 16 percent of whom showed microfilariae.64 It was promptly recommended that these men be returned to one of the islands of the western Pacific or to relatively uninhabited islands where introduction of the disease would be of small consequence.65


A valuable, though expensive, lesson can be learned from the experience with filariasis in World War II. Medical officers should be given all the information available about the diseases in the area into which they go. As information is obtained from one service or area, it should be passed on rapidly, at least as information bulletins, to other officers. While "a little knowledge is a dangerous thing," it is better than none. The War Department technical bulletin on filariasis (p. 138) did not appear until the epidemic was over. The importance of a knowledge of military sanitation for every medical officer in the field, no matter how high his other professional qualifications, was demonstrated again. To this might be added the ineffectiveness of such knowledge unless commanders can be convinced of its importance.

It is highly improbable that any number of men infected overseas will have symptoms or incapacity attributable to filariasis in the future. A few may develop an asymptomatic microfilaremia. A few such cases have been reported.66 This is consistent with Neumann's observations that microfilariae are not commonly found in the peripheral blood before the seventh year after infection. If no longer exposed to reinfection, such microfilariae may persist for 15 years, which apparently is the average life of the worms.67 Such cases, even should they occur, would be so scattered that the chance of establishing a focus of the disease in the United States is negligible.

There is no specific treatment for the acute attacks of filariasis. The sulfonamides and antibiotics are without effect unless bacterial infection is superimposed. Rest and administration of mild analgesics, such as acetylsalicylic acid, during the presence of acute symptoms are all that is required. Of a large number of drugs studied for effect on microfilariae,

64History of Preventive Medicine, Headquarters, U.S. Army Forces, Middle Pacific, ch. 34. [Official record.]
65Swartzwelder, J. C.: Filariasis Bancrofti. In Medical Department, United States Army. Preventive Medicine in World War II. Volume VII. Washington: U.S. Government Printing Office, 1964.
66(1) Eyles, D. E., Hunter, G. W. III, and Warren, V. G.: Periodicity of Microfilariae in 2 Patients With Filariasis Acquired in South Pacific. Am. J. Trop. Med. 27: 203-209, March 1947. (2) Conn, H. C., and Greenslit, F. S.: Filariasis Residuals in Veterans With Report of Case of Microfilaremia. Am. J. Trop. Med. 1: 474-476, May 1952.
67Neumann, H.: Filariasis in White Man. J. Trop. Med. 47: 25-28, June-July 1944.


diethylcarbamazine (Hetrazan) is the most promising.68 It is quite effective in reducing or abolishing microfilaremia. Its effect on adult worms is less definitive.

68(1) Santiago-Stevenson, D., Oliver-Gonzalez, J., and Hewitt, R. I.: Treatment of Filariasis Bancrofti With 1-Diethylcarbamyl, 4-Methylpiperazine Hydrochloride ("Hetrazan"). J.A.M.A. 135: 708-712, 15 Nov. 1947. (2) Kessel, J. F., Thooris, G. C., and Bambridge, B.: Use of Diethylcarbamazine (Hetrazan or Notezine) in Tahiti as an Aid in Control of Filariasis. Am. J. Trop. Med. 2: 1050-1061, November 1953.