CHAPTER XIII
Fort Bragg Fever
Worth B. Daniels, M.D.
The recognition of Fort Bragg fever as a specific new diseaseentity and the ultimate proof of its etiology is a contribution of the U.S. ArmyMedical Department to the science of medicine. The disease was described by Armyclinicians, studied by Army medical personnel with the assistance ofArmy-consigned consultants, transmitted to animals by an Army research worker,and finally proved as to etiology by an Army veterinarian and others working atthe Medical Department Professional Service Schools, Army Medical Center,Washington, D.C.
The story of Fort Bragg fever indicates, too, the superioropportunities which were available to military medical personnel for clinicalresearch. Larger groups of patients with the same disease are more oftenavailable for study in military installations than in civilian institutions. Itis doubtful whether this disease would have been recognized as an entity had theoutbreak occurred in an urban civilian community; there, each patient might havebeen cared for by a different physician and treated in a different hospital,whereas, on an Army post all were concentrated in one hospital under the care ofa closely knit medical service.
RECOGNITION OF A NEW DISEASE
Late in July and early in August 1942, an unusual febrileillness occurred in a group of soldiers at Fort Bragg, N.C.1It shortly became apparent not only that these men had identical symptoms butalso that they all came from a few organizations quarterednear one another in a limited area of the reservation. Between 29 July and 11September, 40 patients with this illness were admitted to the hospital. Thehistory was one of relatively sudden onset characterized by malaise, mildgeneral aching, lumbar pain, severe frontal headaches, and postorbital pain. Onthe first or second day of symptoms, mild respiratory manifestations consistingof coryza, sore throat, pain and soreness in the chest, and cough occurred in 30percent of the patients. The respiratory symptoms were not persistent and werenever suggestive of primary respiratory involvement such as is seen ininfluenza. In about one-fourth of the cases, nausea and vomiting occurred, rarelyaccompanied by abdominal pain. Shaking chills or chilliness and fever developed.The fever was consistently spiking and frequently showed two or more peaks each
1Daniels, W. B., and Grennan, H. A.: Pretibial Fever; An Obscure Disease. J.A.M.A. 122: 361-365, 5June 1943.
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day. Recurrent chills often accompanied the elevations. During the periods oftemperature elevation, severe accentuation of the frontal and postorbital achingwas experienced, but during the periods of lower temperature, the patients feltrelatively well. The fever persisted for 2 to 8 days-averaging 5.4days-withmaximum elevations ranging from 99.8? to 105.6? F. In five patients, atransient elevation of temperature, sometimes as high as 101.4? F., occurredfrom 2 to 7 days after the original febrile period. Stiffness of the neckaccompanied headache in three patients, but examination of the cerebrospinalfluid revealed it to be normal; there was no noticeable relief of headachefollowing lumbar puncture. Adenopathy was not remarkable. A firm spleen waspalpable early in the disease in 95 percent of the patients. Splenomegalypersisted in some patients for as little as 5 days; in others, there was stillnoticeable enlargement after 2 weeks.
The most distinctive feature of the disease, however, was the appearance ofan unusual rash on or about the fourth day of illness. In 60 percent (24) of thepatients, this was bilaterally symmetrical and limited in distribution to thepretibial areas; in an additional 20 percent (8 patients), the pretibial areaswere the primary site of the rash, and a few lesions were scattered elsewhere.Two patients had splotchy, generalized cutaneous manifestations including theanterior surface of both legs. One had a single lesion on the hand. In fivecases, typical in all other respects, no rash was observed. Individual lesionsconsisted of an erythematous localized blush of irregular outline withill-defined borders fading into the surrounding skin. These were often from 2 to5 cm. in their largestdiameter, gradually coalescing with adjacent lesions. The lesions were raised,warmer than the surrounding skin, and sometimes slightly tender to touch. Insome patients, the lesions vaguely resembled erythema nodosum. In two patients,the rash became diffusely distributed over the entire body, and in a few itappeared urticarial. Following the generalized type of rash there was a residualpigmentation which persisted for about 2 weeks. None of the lesions werepurpuric. In most instances, the cutaneous manifestations lasted 2 days, butthey persisted longer in a few patients. Figures 57 and 58 illustrate thepretibial and the generalized forms of the rash.
Biopsies of cutaneous lesions were performed in six typical cases. Theyshowed diffuse edema and a slight to moderate perivascular infiltration withsmall round cells and macrophages. It is clear that drugs played no part in thedevelopment of this rash because only one patient had received sulfonamidetherapy and no other patient received any drug except acetylsalicyclic acid andcodeine. Leukopenia was noted sufficiently often to constitute a typicalfeature; it was present, in all except five patients, at some time during theacute illness. It developed most often between the third and the fifth day ofillness. At the termination of the febrile period, the leukocytes again rose tonormal, and in 14 patients a slight leukocytosis occurred. The number ofleukocytes ranged from 2,800 to 14,000 per cubic millimeter. Dif-
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FIGURE 57.-Erythematous skin lesions over the pretibial regions.
ferential counts usually showed no deviation from normal, although in a fewcases a moderate relative lymphocytosis was present.
Cultures of the blood showed no growth. Agglutinations for ProteusOX-19, Brucella melitensis, thetyphoid-paratyphoid group, and heterophile antibodies were negative. No patienthad been in an area where coccidioidomycosis was endemic. Skin tests usingcoccidioidin antigen were negative in two patients after their recovery.Roentgenograms of the chest were made in many patients, but none showed anyabnormality.
At the termination of the fever, the patients rapidlyreturned to their original healthy state. There was no postfebrile depletion ordepression, and there were no complications.
CASE REPORTS
Case 1-A white soldier, aged 25, admitted to thehospital on 7 August 1942, complained of fever and headache. He had been welluntil 2 days previously, when he felt feverish and chilly. Severe frontalheadache, postorbital pain, and severe backache developed. The next day he feltslightly better, but on the day of admission the symptoms were all accentuated.The temperature was 101? F., the pulse rate 90, and the respiratory rate 20;the leukocytes numbered 8,150 per cu. mm. Nothing unusual was found on physicalexamination. On the fifth day of the disease, the spleen was firm and easilypalpable. Over the pretibial surfaces of both legs, irregular, erythematouslesions were noted; these were faintly tender, warm to touch, andvery slightly raised (fig. 57). The patient's temperature was swinging incharacter and ranged from 99.8? to 104.4? F. without a corresponding rapidityof pulse. The leukocytes numbered 4,900
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CHART 24.-Temperature, pulse, and leukocyte count ofpatient
per cu. mm., with 65 percent polymorphonuclear cells. On the seventh day ofillness, the rash had entirely disappeared, the temperature was normal, and thepatient felt well. The spleen was still palpable at discharge from the hospital.
Case 2-A white soldier, aged 21, admitted to the hospital on 9August 1942-the third day of disease-had as initial symptoms frontal headacheand pain in the feet and legs which later involved various joints. At the onsetthere was nausea without vomiting. Shaking chills had occurred on two occasionsin the 36 hours prior to admission. Physical examination revealed nasalcongestion, pharyngitis, signs of generalized bronchitis, a temperature of 104?F., a pulse rate of 92, and a respiratory rate of 20 (chart 24). The leukocytesnumbered 9,450 per cu. mm. Two hours after admission a rash appeared onthe trunk, neck, and extremities. This consisted of discrete, brilliantlyerythematous, slightly raised, warm plaques varying in size from 1 to 8 cm. in their largest diameter. The rash wasgeneralized (fig. 58) and, as in the other cases, the anterior aspects of bothlegs were involved. During the next few days the temperature ranged from 99? to104.6? F., with very little acceleration of the pulse. The spleen becamepalpable. The rash remained erythematous for 3 days, faded gradually, and left adefinite purplish pigmentation that diminished during the succeeding 2 weeks.The leukocytes were reduced to 4,350 on the sixth day and to 3,700 per cu. mm.on the seventh day, with no abnormality in the differential count. Convalescencewas uneventful.
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FIGURE 58.-Generalized form of skin eruption.
DIFFERENTIAL DIAGNOSIS
A number of different diseases were considered indifferential diagnosis. In the early cases, influenza was suspected, but thetransient character and mildness of the respiratory symptoms, persistence offever, presence of a firm palpable spleen, and the unusual rash eliminated thispossibility. Endemic typhus seemed to be excluded by the short duration of theillness, by the entirely different type of rash, and by the consistentlynegative Weil-Felix reactions with OX-19 at different periods of the illness.Rocky Mountain spotted fever was similarly dismissed from consideration. Therewas no history of bites by ticks in this group. When these patients werestudied, Bullis fever2 had not yet been described, although caseswere being recognized in Texas. Again, absence of bites by ticks and differencein symptomatology indicated that the cases here described were not the same asthose seen at Camp Bullis, Tex. In no cases did adenopathy or thecharacteristic hematological changes of infectious mononucleosis develop. Theduration of the disease, negative cultures of blood and stool, and negativeagglutination re-
2Woodland, J. C., McDowell, M. M.,and Richards, J. T.: Bullis Fever (Lone Star Fever-Tick Fever): An EndemicDisease Observed at Brooke General Hospital, Fort Sam Houston, Texas. J.A.M.A.122: 1156-1160, 21 Aug. 1943.
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actions eliminated the typhoid-paratyphoid group. Theparasites of malaria and relapsing fever were sought, but not found. Denguewas at first thought to be the probable diagnosis. However, as new cases wereobserved, certain prominent features of that disease were consistently absent.No patient had a "camel back" type of fever curve or any postfebriledepletion or depression. The usual vector of dengue, Aedes aegypti, wasnot found in the vicinity. It would be unusual for an outbreak of dengue to belimited to such a small group. The type and the distribution of the rash werenot similar to that seen in dengue. Other denguelike diseases were considered;however, the clinical features of this disease showed definite dissimilarity tothese in one or more important respects. Search of the literature did not reveala description of a clinical entity into which this group of cases would fit.
EPIDEMIOLOGICAL ASPECTS
The organizations from which these soldiers came were quartered in thenorthern third of the populated area of the reservation, near a small stream andits tributaries. Other areas of the post furnished no patients ill with thisdisease; therefore, local environmental factors were thought to be ofetiological importance. There was no single locality off the reservation towhich these men went during the month previous to illness, and they had nocommon meeting place on the reservation. Some of the men had done no swimming,while others swam in several different ponds. Although there was no swimmingplace common to all, more men swam in "McFadgen's Pond" than in anyother place-on or off the reservation.
The factors responsible for the outbreak could not be determined. The medicalinspector of the post made a search for insect vectors that might be suspected.Bedbugs, stableflies, chiggers, ticks, and horseflies were found but for variousreasons were considered unlikely vectors.
During the period of this outbreak, the population ofmosquitoes on the post was very low, but various members of the Culex specieswere found with Culex quinquefasciatus appearing most frequently.This mosquito had been disproved as a carrier of dengue. No representative ofthe dengue vector, A. aegypti, was found, but Aedes atlanticus, Aedescanadensis, and Aedes vexans were. Their presence was thought to beof doubtful importance.
After a decrease in the number of admissions to the hospitalin mid-August, the incidence of the disease again increased sharply. The clinicalpicture, the long period of incubation, and the leukopenia suggested that thedisease was probably due to a virus. The localization of the cases in one areaof the post made it seem probable that it was transmitted by an insect vector.The local medical personnel were unable to carry out studies as to etiology, soThe Surgeon General, U.S. Army, was requested to send especially trainedindividuals to study the outbreak.
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SPECIAL INVESTIGATION
On 3 September 1942, Dr. Norman H. Topping, Passed Assistant Surgeon, U.S.Public Health Service, Maj. (later Lt. Col.) Cornelius B. Philip, SnC, and Dr.John R. Paul, Professor of Preventive Medicine, Yale University School ofMedicine, New Haven, Conn., and Director, Commission on Neurotropic VirusDiseases, Board for the Investigation and Control of Influenza and OtherEpidemic Diseases in the Army, arrived at Fort Bragg to study the disease. TheCommission reviewed the records of the case previously studied and examined thepatients remaining in the hospital. They agreed that the soldiers were ill witha disease unknown to them, but Dr. Topping remembered that an outbreak of adisease with similar features had been encountered in the town of Wrens, Ga., in1940. This illness was locally known as Brushy Creek fever. Inquirylater brought information from Dr. Charles D. Bowdoin,3 who hadobserved these patients and reported them at a later date, that about 35 caseshad occurred. The clinical course and manifestations seemed to be quiteidentical with those at Fort Bragg. A laboratory technician who had made some ofthe cultures of feces was reported as having developed the disease.
The Commission began investigations in regard to the epidemiology andetiology of the disease.4 They showed that, although only 34patients with a rash had been considered to have this disease by medicalofficers of the hospital, the number of cases-in one of the regimentsinvolved-without a rash might have exceeded those with a rash by as much as 50percent. The Commission confirmed the fact that the disease was not spreadevenly throughout the camp population; but, of the 34 cases (with a rash)diagnosed between 27 July and 19 September, 75 percent had occurred in 3regimental units. Practically all of the cases (almost 97 percent with a rash)occurred in troops quartered in the northern third of the developed area. Acanvass was made of four artillery regiments quartered in the southern sectionof the post, and no "missed cases" were found among 4,800 troops.
These features, plus the fact that the rate of attack was particularly highin two units, led the Commission to suspect that some local, althoughunrecognized, environmental feature was responsible. Particular attention waspaid, therefore, to two units. In each of these, an epidemic amounting almost toan explosive outbreak had occurred. These outbreaks were separated by about 3weeks and were limited, to some extent (in the early cases), to a singlecompany.
These explosive epidemics became apparent when a survey of the records ofillness of one unit in particular, namely, the 88th Airborne Infantry,
3Bowdoin, C. D.: A New Disease Entity(?). J.M.A. Georgia 31: 437-438, 442, December 1942.
4Preliminary Report of the Commission forthe Study of an Unidentified Disease at Fort Bragg, N.C., 3-11 Sept. 1942, byDr. Norman H. Topping, P.A. Surgeon, U.S. Public Health Service, Maj. CorneliusB. Philip, SnC, U.S. Army, and Dr. John A. Paul, Yale University School ofMedicine. Submitted to The Surgeon General, U.S. Army, 15 Oct. 1942.
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revealed that there had been a sharp increase of cases of"influenza,""nasopharyngitis," or"fever of undetermined origin" in this regiment during August. Of the33 cases of "influenza," and other diseases, which were reported inAugust, 9 developed a rash after they had been hospitalized and were ultimatelydiagnosed as having Fort Bragg fever. In 14 others, whose hospital records wereavailable for study, the picture was compatible with that of Fort Bragg fever,although the rash was lacking.
It was concluded, therefore, that a nonexanthematous form of this diseaseexisted and (if all forms of the disease were considered) it could appear inexplosive epidemic form resulting in almost 10 percent of the personnel in agiven company being infected within the period of 2 weeks. Factors responsiblefor this type of explosive outbreak were not determined.
Certain informationabout the period of incubation was obtained. Five men probably developed thedisease while they were away from the post and several developed it within a fewdays after their return, following an absence of 10 days on maneuvers onChesapeake Bay. If it is assumed that the disease was not spread by directcontact, the data accumulated would indicate that the incubation period was from10 to 15 days or longer.
The Commission's entomological observations indicated that if parasiticarthropods were vectors of the disease, there were only three that were found orreported in sufficient numbers and of sufficient distribution to be considered.These were stableflies (Stomoxys calcitrans), mosquitoes, and chiggers (Trombiculairritans). These parasites had also been reported to have bitten menstationed in units in the southern part of the post, where none of the casesoccurred.
As to mosquitoes, it was found that a ditched but swampy arm of Tank Creekseparating the two most heavily infected units could have provided the mostavailable source of breeding, but reports of adjacent troops and of sanitarypersonnel indicated insufficient incidence of mosquitoes in both July and earlyAugust to account for the outbreak. The evidence of transmission by mosquitoeswas not considered strong.
Having collected and frozen material for further study, the Commissiondeparted on 11 September to carry out investigations of etiology in theirvarious laboratories.
Search for an etiological agent was carried out by members of the Commissionat the National Institute of Health, U.S. Public Health Service, at the YaleUniversity School of Medicine, and at the Medical Department ProfessionalService Schools.5
The material obtained for study consisting of blood fromacutely sick patients and a variety of insects (including Stomoxys calcitrans)had been frozen and kept on Dry Ice. It was inoculated intoembryonated eggs, guinea
5Final Report of the Commission forthe Study of an Unidentified Disease at Fort Bragg, N.C., 3-11 Sept. 1942, byDr. Norman H. Topping, P.A. Surgeon, U.S. Public Health Service. Maj. CorneliusB. Philip, SnC, U.S. Army, and Dr. John R. Paul, Yale University School ofMedicine. Submitted to The Surgeon General, U.S. Army, 31 Mar. 1943.
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pigs, mice, monkeys, and one chimpanzee. Human transmissionexperiments were tried by inoculating frozen whole blood and by allowing A.aegypti and Aedes albopictus mosquitoespreviously fed on a patient ill with the disease to feed on volunteers. Each oneof these attempts to transmit the disease failed. In retrospect, however, thenegative findings with frozen human material were explained by an importantdiscovery made about 2 years later, when it was shown that the causative agentof this disease is destroyed by freezing. It is small wonder, therefore, thatthe experiments of 1942 wereunsuccessful. It was not until 1st Lt. (later Capt.) Hugh Tatlock, MC, succeededin performing direct transmission experiments with fresh blood in guinea pigs in1944 that the disease wassuccessfully transmitted.
Outbreaks similar to that of 1942 occurredduring the summers of 19436 and 19447among soldiers quartered in the same area of thepost. In 1943, a rickettsia-like organism was recovered by Tatlock8 fromthree of five guinea pigs injected with fresh blood from a patient ill with thedisease. Attempts were made to show that this agent was concerned in theetiology of the disease. However, subsequent studies indicated that thisorganism was undoubtedly of guinea pig origin and not concerned in the etiologyof Fort Bragg fever.
In the summer of 1944, Tatlockinjected two guinea pigs and two Syrian hamsters intraperitoneally with bloodfreshly drawn from a patient ill for 4 dayswith the disease.9 Both guinea pigs developed fever(105? to 106?F.) 8 days after inoculation. Both guinea pigs were found dead onthe 10th day. No passage was attempted from the hamsters. Serial transmission ofthe fever-producing agent in guinea pigs was accomplished by the intraperitonealinjection of citrated blood on the first day of fever. The incubation period was4 to 8 days and fever persisted from 2 to 4 days. More than 70 passagesproduced no increase in virulence of the agent. No gross abnormalities werefound in sacrificed guinea pigs. Histological sections of the liver showed areasof focal necrosis. No inclusion bodies or Rickettsia wereseen in sections.
Tatlock found the agent capable of infecting guinea pigs,rabbits, and Syrian hamsters by both intraperitoneal and intracerebralinoculation. The disease transmitted was uniformly fatal for hamsters.Intravenous inoculation of 11-day chick embryos was accomplished. From theseinfected eggs, the agent was propagated by the yolk-sac route, and fresh tissuesuspensions were infective for hamsters in 1 to 100,000 dilution. The agentpassed a Corning fritted glass filter but failed to pass a single Seitz pad.Tissue emulsions in sterile skim milk, frozen rapidly and maintained at -70?C.,
6Personal observation of the author.
7Personal communication, J. M. Kinsman, to the author.
8Tatlock, H.: A Rickettsia-Like Organism RecoveredFrom Guinea Pigs. Proc. Soc. Exper. Biol. & Med. 57: 95-99, October 1944.
9Tatlock, H.: Studies on a Virus From a Patient WithFort Bragg Fever (Pretibial Fever). J. Clin. Investigation 26: 287-297, March 1947.
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retained viability. However, blood, whole tissues, or tissuessuspended in broth lost infectivity when stored for 24 hoursat 20? C., 4? C., or at -70? C.in sealed glass ampules.
Sera from five patients with Fort Bragg fever were used in protection tests.Neutralization was obtained in two patients with convalescent, but not withacute, sera. Comparable results were obtained with two sets of sera frominfected guinea pigs.
By early 1945, Captain Tatlockhad brought his studies to a point where he and others interested in the diseasewere confident that Fort Bragg fever was due to a well-characterized filtrablevirus unrelated to any other known virus. At this juncture, he was ordered toWalter Reed General Hospital, Army Medical Center, for clinical duties butmaintained the agent there by passages and by storage, frozen in an emulsion ofmilk.
During the summer months of 1945, nopatients with this disease were admitted to the hospital at Fort Bragg. It is ofinterest that a large part of the post area in which patients had previouslyseemed to acquire the disease was unoccupied except for a period of "a weekor two."10
Isolated reports appeared of single cases of Fort Bragg feverin Connecticut,11 New York,12 andCalifornia.13 From the descriptions given,these patients may have had this disease, although it would seem difficult tomake an absolute diagnosis in the absence of an outbreak.
ADDENDUM
In the spring of 1946, CaptainTatlock was ordered on detached service to Cincinnati, Ohio, where, through thecooperation of Dr. Albert B. Sabin and of the Longview State Hospital, he beganstudies in transmission among a group of patients undergoing fever therapy. He inoculatedthree patients intramuscularly and intracutaneously with a 10-percent suspensionof infected, embryonated chick liver in saline. This material had been through80 passages in guinea pigs and 23 passages14 inembryonated eggs. After an incubation period of 8 to 9 days all three patientsdeveloped a short febrile illness. Successful inoculation of three otherpatients, using freshly defibrinated pooled blood from the previous patients,was accomplished, and a third passage was successful in seven of eight otherindividuals. All but one of the latter patients, after an incubation periodcomparable to that of the natural disease (8 to 14 days),developed fever, and the majority exhibited the clinical picture of Fort Braggfever with rash and leukopenia. For the third passage, two patients immune to"New Guinea C" strain of dengue fever virus, two immune to the"Hawaiian" strain of virus, and two immune
10Personal communication, J. H. Dingle, to the author.
11Lipscomb, L. L., andMcMahon, J. L.: Pretibial Fever. J.A.M.A. 128: 90-91, 12 May 1945.
12Greenfield, I.: Pretibial Fever; ANew Disease Entity. Urol. & Cutan. Rev. 47: 435-436, July 1943.
13Personal communication, G. Cheney,to the author.
14Seefootnote 9, p. 445.
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to the "Middle East-Sicilian" type of sandfly fever virus wereused. All were found susceptible to the "virus" of Fort Bragg fever.
"Viremia" was demonstrated in these patients by the immediateinoculation of fresh, defibrinated blood into young hamsters. The"virus" appeared in the blood of these patients shortly before theonset of fever and disappeared rapidly thereafter.
It now appeared clear to all interested in the disease that the"virus" isolated by Tatlock from a case of Fort Bragg fever in 1944 was a new and distinct agent capable of producing the classicalmanifestations of the natural disease when inoculated into man.
In 1947, in New Haven, Melnick and Paul15 inoculated fourchimpanzees intracutaneously and subcutaneously, using the "virus"isolated by Captain Tatlock. These animals developed a disease similar in manyrespects to the experimental disease transmitted to humans by Tatlock, andsubsequent bleedings showed that they had developed neutralizing antibodies.When "virus" inactivated by freezing was inoculated into fivechimpanzees, no disease or neutralizing antibodies developed. Two of theseanimals were later given active "virus" and both developed antibodies.Two animals were studied for "viremia" during the period of fever.This was demonstrated in one of the animals by transmission to a chimpanzee andin the other by transmission to young hamsters.
During the ensuing years, the "virus" of Fort Bragg fever wasmaintained in several laboratories. The possibility that this agent might be a Leptospirawas considered several times by Gochenour, Smadel, and others at the ArmyMedical Service Graduate School, Walter Reed Army Medical Center.16However, results obtained with methods then employedfailed to support this idea.
Later, a large collection of leptospiral strains wasassembled by this group. In the fall of 1951, Gochenour, an Army veterinarian-with Smadel and othercoworkers-found that with antigens preparedfrom these strains convalescent and immune sera of victims of Fort Bragg fevergave a high titer of agglutinating antibodies against Leptospira autumnalis. Withthis lead, a leptospiral organism was recovered by culture from the 365thpassage of the Fort Bragg agent since its original isolation.Cross-agglutination tests showed that the Fort Bragg agent was essentiallyindistinguishable from Lept. autumnalis Akiyami A, the cause of autumnalfever in Japan and other areas of the Far East. There was then no doubt that Lept.autumnalis was being carried in this laboratory as the "virus" ofFort Bragg fever. Obviously, it was of the utmost importance to learn whetherthis was a contaminant or whether it really originated from patients with thedisease at Fort Bragg.
15Melnick, J. L., and Paul, J. R.: Experimental FortBragg Fever (Pretibial Fever) in Chimpanzees. Proc. Soc. Exper. Biol. & Med.67: 263-268, March 1948.
16Gochenour, W. S., Jr., Smadel, J. E., Jackson, E. B., Evans, L. B., and Yager, R. H.: LeptospiralEtiology of Fort Bragg Fever. Pub. Health Rep. 67: 811-813, August 1952.
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Paired sera from Melnick and Paul's four euphoniously named chimpanzees-Rosebud,Mary Lou, Hickory, and Catawba-showed high titers of agglutinins or neutralizingantibodies against Lept.autumnalis in the convalescent, but none in theacute, sera. Paired sera from six of Captain Tatlock's patients infected inCincinnati gave the same results.
Fortunately, paired sera from five of the original soldiers who had been bledby Tatlock in 1944 werestill safe in the Deepfreeze. Three of these patients were found to havedeveloped neutralizing antibodies and leptospiral agglutinins. Two who failed to develop neutralizing antibodies in CaptainTatlock's experiments also failed to agglutinate Lept. autumnalis.
It is of great interest that three lots of hyperimmune rabbit sera-oneprepared in 1947 fromthe hamster line, another in 1951 from cultured Leptospirae of the Fort Bragg agent, and a third from cultures ofLept.autumnalis Akiyami A-protected hamsters against100,000 LD50 of the Fort Bragg Leptospira.
Stored sera from 45 Fort Bragg patients ill in 1943 or1944, though not paired, were studied. Sixteen of these gaveclear-cut serological evidence of infection with Fort Bragg Leptospira.
Fort Bragg fever then is caused by a member of the Lept.autumnalis group. No member of this group waspreviously known to exist in the United States. This disease takes its placewith Weil's disease, swineherd's disease, canicola fever, and other leptospiral diseases and is a contributionof Army medical investigation to medicine.
