CHAPTER VII
Psittacosis
Joseph E. Smadel, M. D.
A single case of psittacosis was recorded amongUnited States Army personnel duringWorld War II. The history of this case is of sufficient interest towarrant a summary.
Case report.-A 51-year-old white officerwas admitted to the Station Hospital, Port ofEmbarkation, San Francisco, Calif., on 3 March 1944. His complaints onadmission werevomiting and diarrhea followed by dizziness and headache of about 3days' duration, also atemperature of 104 o F.
On physical examination,the patient had tenderness deep in the right upper quadrant ofthe abdomen and an unsteady gait associated with a horizontalnystagmus. Lumbar puncture andstool cultures were negative; the urine showed moderate albuminuriawith granular casts and afew white cells in the sediment. The white cell count was 5,450.Agglutinations for typhoid werepositive at dilutions of 1:640 and at 1:20 for paratyphoid. A chestroentgenogram revealed anincrease in confluent linear density extending from the right hilum tothe right lower lung field,interpreted as due to an inflammatory process such as an atypicalpneumonia.
On 7 March, the patient was transferred to Letterman General Hospital, San Francisco. Physical examination disclosed him to be acutely ill with moderate dyspnea and slight cyanosis. There was marked abdominal distention and dehydration. Auscultation of the lungs showed subcrepitant and crepitant rales involving the entire right lower lobe and, to a lesser extent, the left lower lobe. The liver extended 4 cm. below the right costal margin.
Laboratory studies were as follows: Red blood count, 4.3 million; hemoglobin, 83 percent; white blood count, 6,700 with 57 percent neutrophils, 30 percent lymphocytes, 1 percent monocytes, 1 percent eosinophils, and 1 percent basophils. Urine showed 3 plus albuminuria, negative sugar, few fine and coarse granular casts, 5 to 7 white blood cells, and 1 to 3 red blood cells over high-power fields. Agglutinations for typhoid and paratyphoid were nondiagnostic; for tularemia and brucellosis, negative. Stool examination and culture were not, significant. Repeat leukocyte counts showed a persistently normal white blood count ranging from 5,450 to 12,100, the latter obtained on the day prior to death. Urinalyses remained essentially the same. Blood urea nitrogen and chlorides were normal. Total proteins were 4.35 gm. per 100 cc., with 2.35 gm. albumin and 1.30 gm. globulin per 100 cc. Cold agglutinins were negative. A roentgenogram of the chest showed an increase in the confluent density in the right lower lobe, and flat plate of the abdomen revealed a considerable amount of gaseous distention of the large and small intestines.
Despite intensive therapy with blood transfusion, parenteral fluids, and supportive measures to combat the distention and dyspnea, the patient's course continued febrile and he died on 14 March.
At autopsy, a definite patchy pneumonitis was found involving the left upper and lower lobes, and the right middle and lower lobes.On microscopic
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section, there was a diffuse but patchy pneumonic involvementcharacterized mainly by largemononuclear leukocytes filling the distended alveoli with activephagocytosis of nuclearparticles. Different stages of pneumonia were seen with some areasshowing early organization.Lung smears were examined for elementary bodies, but no definitelydiagnostic elementarybodies could be seen, though a few macrophages contained small granularobjects which stainedred. The gastrointestinal tract showed a severe acute gastroenteritisinvolving the stomach,duodenum, jejunum, ileum, and colon.
Lung tissue obtained at autopsy was examined by Dr. Gordon Meiklejohn at the University of California, Berkeley, with the following report:
A 20 percent suspension of lung tissue in broth was inoculated intranasally in 0.45 cc. amounts into 2 adult western cotton rats under ether anesthesia. On the second day, they began to appear sick and dyspneic and by the fourth day were moribund and were sacrificed. Both showed extensive pulmonary consolidation, greyish in color. Impression smears of the lungs stained by the method of Macchiavello showed very large numbers of intracellular elementary bodies, frequently in unusually large clusters. The control cotton rats from the same stock inoculated at the same time with 0.45 cc. of broth showed no evidence of disease.
Six white mice were inoculated intracerebrally with 0.03 cc. of the same suspension. One died on the second day. The remaining 5 died between the fourth and sixth day and smears showed rather small numbers of elementary bodies.
Serum taken on theday of death was tested against lymphogranuloma venereum antigen forcomplement fixationwith the following results: 1 to 6, 4 plus; 1 to 12, 3 plus; 1 to 24, 1plus; 1 to 48, 0; New York strain, 0; serumcontrol, 0. The same serum had a cold agglutination titer of less than10.
Dr. K. F. Meyer also recovered a psittacosis-type virus from another portion of the lung tissue obtained at autopsy. These results suggested that the patient's pneumonia was due to a virus in the psittacosis-like group.1
Complement fixation tests were done at theLetterman General Hospital on blood obtainedshortly before death. The results were:
Complement fixation with lygranum antigen: 1 to 5, 4 plus; 1 to 10, 5 plus; 1 to 20, 4 plus; 1 to 40, 3 plus; 1 to 80, 1 plus; 1 to 160, 0; complement fixation with psittacosis antigen (Plotz antigen, Army Medical School No. 6, dated 4 May 1943) : 1 to 5, 4 plus; 1 to 10, 4 plus; 1 to 20, 4 plus; 1 to 40, 4 plus; 1 to 80, 0; 1 to 160, 0.
Epidemiologic studies revealed that this officerwas a transport commander on the John Lykeswhich had left New York on 20 December 1943, and had arrived at SanFrancisco on 15February 1944, after a 6-day stopover from 20 to 26 January at Noumea,New Caledonia. As faras was known, he had had no contact with birds, although it was quitecommon for members ofthe crew to bring canaries onto the ship to be carried back to theUnited States for pets. Thedeceased officer had lived aboard ship until the time of his hospitaladmission and was notknown to have visited any place in San Francisco harboring parrots orother birds. The questionwas raised as to whether the ship lead ever been used fortransportation of birds with a view todetermining whether
1 Letter, Dr. K. F.Meyer to Editorial Office, History of Preventive Medicine, U. S. Army,in World War 11, 6Aug. 1951.
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possible dust from bird droppings might have, been a source of theinfection, but no informationcould be obtained. As far as is known, no other crew members of the JohnLykes had become illwith a similar illness.
EPIZOOTICS
Epizootics causedby members of the psittacosis group of viruses occurred in carrierpigeonsused by the Signal Corps 2 and were ofsome importance in the war effort. During the period ofmilitary mobilization, when primary atypical pneumonia was a matter ofconsiderable concern tothe Medical Corps, the possibility that this disease might be caused byone of the psittacosisagents was carefully investigated.3No evidence of such an etiologic relationship wasestablished then or in subsequent studies on this disease whichcontinued to plague the troops inthe United States and overseas, especially in the European Theater ofOperations.
Observations on primary atypical pneumonia among civilians in the New York metropolitan area during 1941 had shown that an appreciable proportion of these patients actually had psittacosis and had apparently contracted their disease as a result of association with flocks of pigeons in which epizootic psittacosis was present.4 Since enzootic psittacosis exists in practically all flocks of pigeons examined to date 5 and since the disease flares to epizootic stages from time to time, it appeared desirable to study the relation of the avian to the human disease among birds and pigeoneers of the Signal Corps.
The 2d Platoon,280 Signal Pigeon Company (mission to train and supply carrier pigeons)stationed at Tidworth, England, was under almost constant observationby the Virus Division ofthe 1st Medical General Laboratory from January 1943 to March 1945.During this period, therewere a series of sharp epizootics of psittacosis among the flocks ofthe company,6 but no typicalor atypical cases of psittacosis occurred among the personnel of thecompany, despite the factthat many members of the organization were in intimate contact with thesick birds.
2 Smadel, J. E., Jackson, E. B.,and Harman, J. W.: A New Virus Disease of Pigeons; Recovery of theVirus.J.Exper. Med. 81: 385-398, April 1945.
3 Dingle, J. H., Abernethy, T. J.,Badger, G. F., Buddingh, G. J., Feller, A. E., Langmuir, A. D.,Ruegsegger, J. M.,and Wood, W. B.: Primary Atypical Pneumonia, Etiology Unknown.War Med.3: 223-248, March 1943.
4 Smadel, J. E.: Atypical Pneumonia andPsittacosis. J. Clin. Investigation 22: 57-65, January 1943.
5 (1) Coles, J. D. W. A.:Psittacosis in Domestic Pigeons.Onderstepoort J. Vet. Science &Animal Industry 15 (1and 2): 141-148, July and October 1940. (2) Eddie, B., andFrancis, T., Jr.: Occurrence of Psittacosis-like Infection inDomestic and Game Birds of Michigan.Proc. Sec. Exper. Biol. & Med.50:291-295, June 1942. (3) Meyer, K. F.,Eddie, B., and Yanamura, H. Y.: Ornithosis(Psittacosis) in Pigeons and Its Relation to Human Pneumonitis. Proc.Soc. Exper. Biol. & Med. 49: 609-615, April 1942. (4) Blount,W. P.: Psittacosis in Pigeons; A DiseaseCommunicable to Man: An Outbreak in Army Pigeons.J. Roy. Army Vet.Corps 15: 81-83, August 1944; andCanad. J. Comp. Med. 8: 260-264, September 1944. (5)Zichis, J., Shaughnessy, H. J., and Lemke, C.: Isolation ofPsittacosis-like Viruses From Chicago Pigeons.J. Bact. 51: 616-617, May1946. (6) Davis, D. J., and Ewing, C. L.:Recovery of Ornithosis Virus From Pigeons in Baltimore, Maryland. Pub.Health Rep. 62: 1484-1488, 10 Oct. 1947.(7) Labzoffsky, N. A.: Ornithosis Among "Wild" Pigeons inOntario.Canad. J. Pub. Health 38:187-192, April1947. (8) Winsser, J.: Isolation of Ornithosis From Pigeons in TheNetherlands. Antonie van Leeuwenhoek 15 (2):86-90,1949.
6(1) Annual Reports, 1st Medical GeneralLaboratory, 1944, 1945. (2) See footnote 2.
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Two observationscontributed to an explanation of the absence of clinical disease amongthepigeoneers. In the first place, most of the technical personnelresponsible for the care andtraining of the birds had been pigeon fanciers in civilian life, hencethey had had ampleopportunity for prior exposure to the pigeon strain of psittacosisvirus. In the second place,evidence that subclinical infection had taken place in the personnel ofthis company wasforthcoming when it was shown that the sera of approximately one-thirdof the men possessedcomplement-fixing antibodies against the psittacosis-lymphogranulomavenereum group ofviruses. In interpreting these serologic data, several points should beborne in mind: (1) The testfails to differentiate between antibodies elicited by psittacosis virusand the closely related virusof lymphogranuloma venereum; (2) antibodies against thepsittacosis-lymphogranulomavenereum group persist in low titer for long periods of time; (3) theprevalence of a stationarylow titer of these antibodies in an unselected small group of Negrotroops with atypicalpneumonia at Camp Claiborne, La., in 1941 was 46 percent, whereas theprevalence in whitetroops with the same disease at the same post was 4 percent; 7 and (4) personnel of the 280thSignal Pigeon Company were all white. With these points in mind, itseemed reasonable toassume that the majority of the pigeoneers with complement-fixingantibodies against thepsittacosis-lymphogranuloma venereum group of viruses had had previousexposure topsittacosis virus and had suffered a subclinical infection orunrecognized disease. On the otherhand, it was assumed that the high prevalence ofpsittacosis-lymphogranuloma venereumantibodies in Negro troops at Camp Claiborne was the result of exposureto lymphogranulomavenereum.
Civilian outbreaks of psittacosis have been characterized by a high degree of communicability between infected birds and man and, in some, instances, by a moderately high degree of communicability from man to man.8 In contrast to this general experience, there is evidence that one laboratory officer, who carried psittacosis virus in his sputum, did not, so far as is known, transmit the agent to other military personnel. This officer contracted psittacosis in 1938 as a result of work in a laboratory where the virus was being studied. He entered the Army early in the war and was released from active duty in April 1946. He was hospitalized in Letterman General Hospital in February 1946 because of a chronic cough and, at that time and on subsequent occasions, psittacosis virus was recovered from his sputum.9 The officer was not aware of exposure to psittacosis after joining the military service, and the most probable explanation for the presence of virus in his respiratory tract is that he was a
7 See footnote 3, p. 143.
8(1) See footnote 4, p. 143. (2) Meyer,k. F.: Pigeons and Barn Yard Fowls as Possible Sources of HumanPsittacosis or Ornithosis. Schweiz. med. Wehnschr. 71: 1377-1379, 1Nov.1941. (3) Meyer, IL. F.: TheEcology ofPsittacosis and Ornithosis (De Lamar lecture).Medicine 21: 175-206, May1942.
9 Surgical RecordNo. S-26265, Tissues of Animals Inoculated WithPatient's Sputum. (Filed at the Armed ForcesInstitute of Pathology under Accession No. 168625.)
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chronic carrier of the agent.10 Althoughsuch a chronic carrier state is frequently observed inbirds or laboratory animals,11 itsoccurrence in man had not been observed previously.
Anotherobservation in the Army was also a little surprising in view ofprevious experience.Large numbers of parrots and related birds were acquired as pets bypersonnel in the Pacific andother theaters. These birds lived in close contact with their masters,and numerous attempts weremade to smuggle them into the United States by returning troops.Occasional infections withpsittacosis might have been expected under these conditions, yet notone was reported. Whetherthe single psittacosis death among military personnel (the transportofficer previouslymentioned) was a result of infection from such an exposure is unknown.
10 Meyer,K;. F., and Eddie, B.: Human Carrier of the Psittacosis Virus.J.Infect. Dis. 88: 109-125, March-April1951.
11 Quan, S. F.,Meyer, K. F., and Eddie, B.: Attempts to Cure. ParakeetPsittacosis Carriers With Aureomycin andPenecillin. J. Infect. Dis. 86: 132-135, March-April 1950.
