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Chapter 7 - Psittacosis




Joseph E. Smadel, M. D.

A single case of psittacosis was recorded among United States Army personnel during World War II. The history of this case is of sufficient interest to warrant a summary.

Case report.-A 51-year-old white officer was admitted to the Station Hospital, Port of Embarkation, San Francisco, Calif., on 3 March 1944. His complaints on admission were vomiting and diarrhea followed by dizziness and headache of about 3 days' duration, also a temperature of 104 o F.

On physical examination, the patient had tenderness deep in the right upper quadrant of the abdomen and an unsteady gait associated with a horizontal nystagmus. Lumbar puncture and stool cultures were negative; the urine showed moderate albuminuria with granular casts and a few white cells in the sediment. The white cell count was 5,450. Agglutinations for typhoid were positive at dilutions of 1:640 and at 1:20 for paratyphoid. A chest roentgenogram revealed an increase in confluent linear density extending from the right hilum to the right lower lung field, interpreted as due to an inflammatory process such as an atypical pneumonia.

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


section, there was a diffuse but patchy pneumonic involvement characterized mainly by large mononuclear leukocytes filling the distended alveoli with active phagocytosis of nuclear particles. Different stages of pneumonia were seen with some areas showing early organization. Lung smears were examined for elementary bodies, but no definitely diagnostic elementary bodies could be seen, though a few macrophages contained small granular objects which stained red. The gastrointestinal tract showed a severe acute gastroenteritis involving 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 the day of death was tested against lymphogranuloma venereum antigen for complement fixation with the following results: 1 to 6, 4 plus; 1 to 12, 3 plus; 1 to 24, 1 plus; 1 to 48, 0; New York strain, 0; serum control, 0. The same serum had a cold agglutination titer of less than 10.

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 the Letterman General Hospital on blood obtained shortly 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 officer was a transport commander on the John Lykes which had left New York on 20 December 1943, and had arrived at San Francisco on 15 February 1944, after a 6-day stopover from 20 to 26 January at Noumea, New Caledonia. As far as was known, he had had no contact with birds, although it was quite common for members of the crew to bring canaries onto the ship to be carried back to the United States for pets. The deceased officer had lived aboard ship until the time of his hospital admission and was not known to have visited any place in San Francisco harboring parrots or other birds. The question was raised as to whether the ship lead ever been used for transportation of birds with a view to determining whether

1 Letter, Dr. K. F. Meyer to Editorial Office, History of Preventive Medicine, U. S. Army, in World War 11, 6 Aug. 1951.


possible dust from bird droppings might have, been a source of the infection, but no information could be obtained. As far as is known, no other crew members of the John Lykes had become ill with a similar illness.


Epizootics caused by members of the psittacosis group of viruses occurred in carrier pigeons used by the Signal Corps 2 and were of some importance in the war effort. During the period of military mobilization, when primary atypical pneumonia was a matter of considerable concern to the Medical Corps, the possibility that this disease might be caused by one of the psittacosis agents was carefully investigated.3 No evidence of such an etiologic relationship was established then or in subsequent studies on this disease which continued to plague the troops in the United States and overseas, especially in the European Theater of Operations.

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 observation by the Virus Division of the 1st Medical General Laboratory from January 1943 to March 1945. During this period, there were a series of sharp epizootics of psittacosis among the flocks of the company,6 but no typical or atypical cases of psittacosis occurred among the personnel of the company, despite the fact that many members of the organization were in intimate contact with the sick birds.

2 Smadel, J. E., Jackson, E. B., and Harman, J. W.: A New Virus Disease of Pigeons; Recovery of the Virus.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 and Psittacosis. 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 (1 and 2): 141-148, July and October 1940. (2) Eddie, B., and Francis, T., Jr.: Occurrence of Psittacosis-like Infection in Domestic 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 Disease Communicable to Man: An Outbreak in Army Pigeons.J. Roy. Army Vet. Corps 15: 81-83, August 1944; and Canad. J. Comp. Med. 8: 260-264, September 1944. (5) Zichis, J., Shaughnessy, H. J., and Lemke, C.: Isolation of Psittacosis-like Viruses From Chicago Pigeons.J. Bact. 51: 616-617, May 1946. (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 in Ontario.Canad. J. Pub. Health 38:187-192, April 1947. (8) Winsser, J.: Isolation of Ornithosis From Pigeons in The Netherlands. Antonie van Leeuwenhoek 15 (2): 86-90,1949.

6(1) Annual Reports, 1st Medical General Laboratory, 1944, 1945. (2) See footnote 2.


Two observations contributed to an explanation of the absence of clinical disease among the pigeoneers. In the first place, most of the technical personnel responsible for the care and training of the birds had been pigeon fanciers in civilian life, hence they had had ample opportunity for prior exposure to the pigeon strain of psittacosis virus. In the second place, evidence that subclinical infection had taken place in the personnel of this company was forthcoming when it was shown that the sera of approximately one-third of the men possessed complement-fixing antibodies against the psittacosis-lymphogranuloma venereum group of viruses. In interpreting these serologic data, several points should be borne in mind: (1) The test fails to differentiate between antibodies elicited by psittacosis virus and the closely related virus of lymphogranuloma venereum; (2) antibodies against the psittacosis-lymphogranuloma venereum group persist in low titer for long periods of time; (3) the prevalence of a stationary low titer of these antibodies in an unselected small group of Negro troops with atypical pneumonia at Camp Claiborne, La., in 1941 was 46 percent, whereas the prevalence in white troops with the same disease at the same post was 4 percent; 7 and (4) personnel of the 280th Signal Pigeon Company were all white. With these points in mind, it seemed reasonable to assume that the majority of the pigeoneers with complement-fixing antibodies against the psittacosis-lymphogranuloma venereum group of viruses had had previous exposure to psittacosis virus and had suffered a subclinical infection or unrecognized disease. On the other hand, it was assumed that the high prevalence of psittacosis-lymphogranuloma venereum antibodies in Negro troops at Camp Claiborne was the result of exposure to lymphogranuloma venereum.

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 Human Psittacosis or Ornithosis. Schweiz. med. Wehnschr. 71: 1377-1379, 1 Nov. 1941. (3) Meyer, IL. F.: The Ecology of Psittacosis and Ornithosis (De Lamar lecture).Medicine 21: 175-206, May 1942.

9 Surgical Record No. S-26265, Tissues of Animals Inoculated With Patient's Sputum. (Filed at the Armed Forces Institute of Pathology under Accession No. 168625.)


chronic carrier of the agent.10 Although such a chronic carrier state is frequently observed in birds or laboratory animals,11 its occurrence in man had not been observed previously.

Another observation in the Army was also a little surprising in view of previous experience. Large numbers of parrots and related birds were acquired as pets by personnel in the Pacific and other theaters. These birds lived in close contact with their masters, and numerous attempts were made to smuggle them into the United States by returning troops. Occasional infections with psittacosis might have been expected under these conditions, yet not one was reported. Whether the single psittacosis death among military personnel (the transport officer previously mentioned) 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-April 1951.

11 Quan, S. F., Meyer, K. F., and Eddie, B.: Attempts to Cure. Parakeet Psittacosis Carriers With Aureomycin and Penecillin. J. Infect. Dis. 86: 132-135, March-April 1950.