Abstract A pulmonary lesion of sheep, apparently of infectious origin but resembling a tumor in its morphologic characteristics, has been known since about 1891.1 It has received such varying names as jagziekte, epizootic adenomatosis, pulmonary adenomatosis and infectious adenomatosis. Very similar and probably identical conditions have been reported under the titles of verminous pneumonia and Montana progressive pneumonia of sheep. A considerable incidence has been found in areas as widely separated as South Africa, Saxony, England, Iceland and Montana. Similar changes have been seen in horses3 and guinea pigs,4 and as early as 1903 Löhlein5 found a picture resembling it in a 69 year old woman. Since that time, the veterinary literature on the subject has become voluninous, and there have been several other human cases recorded. REPORT OF A CASE A white man aged 42 was admitted to the Wisconsin General Hospital April 19, 1941, with References 1. Eber, A.: Bericht über das Veterinärwesen im Königreich Sachsen für das Jahr 1891, p. 43 2. cited by Pallaske.2 3. Pallaske, G.: Zur Kenntnis der sogennaten Adenomatose oder der multiplen Adenome d'un corynebacille diphtéroïde , Bull. Assoc. franç. p. l'étude du cancer 15:212-237, 1926. 4. Theiler, A.: Jaagsiekte in Horses , in Seventh and Eighth Reports of the Director of Veterinary Research, Union of South Africa, April 1918, p. 59. 5. Grumbach, A.: Tumeurs épithéliales du poumon chez le cobaye à la suite d'injection d'un corynebacille diphtéroïde , Bull. Assoc. franç. p. l'étude du cancer 15:212-237, 1926. 6. Löhlein, M.: Cystisch-papillärer Lungentumor , Verhandl. d. deutsch. path. Gesellsch. 12:111-115, 1908. 7. Ewing, J.: Neoplastic Diseases , ed. 4, Philadelphia, W. B. Saunders Company, 1940, p. 874. 8. Cowdry, E. V.: Comparative Pathology of South African Jaagsiekte and Montana Progressive Pneumonia of Sheep , J. Exper. Med. 45:571-585 ( (April) ) 1927Crossref 9. Studies on the Etiology of Jaagsiekte , Cowdry J. Exper. Med. 42:335-345 ( (Sept.) ) 1925.Crossref 10. Dungal, N.: Epizootic Adenomatosis of the Lungs of Sheep: Its Relation to Verminous Pneumonia and Jaagsiekte , Proc. Roy. Soc. Med. 31:497-505 ( (March) ) 1938. 11. Pallaske.2 12. Oberndorfer, S.: Zellmutationen und multiple Geschwulstenstehungen in den Lungen , Virchows Arch. f. path. Anat. 275:728-737, 1930.Crossref 13. Helly, K.: Ein seltener primärer Lungentumor , Ztschr. f. Heilk. 28:105-110, 1907. 14. Aynaud, M.: Origine vermineuse du cancer pulmonaire de la brebis , Compt. rend. Soc. de biol. 95:1540-1542, 1926. 15. Bonne, C.: Morphological Resemblance of Pulmonary Adenomatosis (Jaagsiekte) in Sheep and Certain Cases of Cancer of the Lung in Man , Am. J. Cancer 35:491-501 ( (April) ) 1939. 16. Richardson, G. O.: Adenomatosis of the Human Lung , J. Path. & Bact. 51:297-298 ( (Sept.) ) 1940. 17. Briese: Zur Kenntnis des primären Lungenkarzinoms, mit statistischen Angaben , Frankfurt. Ztschr. f. Path. 23:48-55, 1920. 18. Dungal, N., and Taylor, E. L.: Epizootic Adenomatosis in the Lungs of Sheep: Comparison with Jaagsiekte, Verminous Pneumonia and Progressive Pneumonia , J. Comp. Path. & Therap. 51:46-68 ( (March 31) ) 1938. 19. de Kock, G.: Are the Lesions of Jaagsiekte in Sheep of the Nature of a Neoplasm? Ann. Rep. Dir. Vet. Serv. (sect. V-IX) 2:611-641, 1929 20. Further Observations on the Etiology of Jaagsiekte in Sheep , de Kock Ann. Rep. Dir. Vet. Serv. 2:1169-1183, 1929.

<jats:p>This datasheet on pulmonary adenomatosis covers Identity, Overview, Associated Diseases, Pests or Pathogens, Distribution, Hosts/Species Affected, Diagnosis, Pathology, Epidemiology, Impacts, Prevention/Control, Further Information.</jats:p>

Pulmonary Adenomatosis 1 Lester W. Paul , M.D. and Gorton Ritchie , M.D. Madison, Wis. ↵ 1 From the Departments of Radiology and Pathology, The University of Wisconsin Medical School, Madison, Wis. Read by title at the Thirty-first Annual Meeting of the Radiological Society of North America, Chicago, Ill., Nov. 9–10, 1945. Excerpt Pulmonary adenomatosis in man is a rare disease of the lungs characterized by the development of multiple nodular adenomatous tumors or by a diffuse hyperplasia of the pulmonary alveolar lining cells. Typically the disease spreads throughout both lungs, interfering greatly with the gaseous exchange in the alveoli and eventually causing death, often with a terminal pneumonia and without the occurrence of metastases elsewhere in the body. The lesion has stimulated considerable speculation and interest, chiefly among pathologists, because of its close resemblance histologically to an infectious disease of the lungs which is widely encountered in sheep and to a lesser degree in some other animals. The present report is made for the purpose of reviewing the pathologic and clinical aspects of the disease, and more particularly the roentgen features, and to report our experiences in four cases, three of which have not previously been recorded in the literature. A fifth case will be discussed briefly because of interesting findings on histologic study. Writers on the subject of human pulmonary adenomatosis have been impressed by its resemblance to the condition found in sheep and known variously as jaagsiekte, epizootic adenomatosis, Montana progressive pneumonia of sheep, etc. (3, 9, 12). This disease has been endemic in many areas throughout the world and has been the subject of considerable study. There is sufficient evidence to indicate that it is of infectious origin, though the causative organism has not as yet been found. That a virus is responsible is the opinion of those who have made extensive studies. In 1939, Bonne (3) described a peculiar tumor-like process of the lungs found in a 30-year-old Chinese, characterized by a diffuse involvement of the alveolar walls of most of both lungs and a replacement of the alveolar cells by darkly staining cells in which mitoses were frequently seen. These cells lined the alveolar sacs and often protruded into their lumina forming papillary buds. There was practically no invasive growth or necrosis, and no metastases were present. Bonne noted the close resemblance to jaagsiekte in sheep and commented on the possible relationship. He did not believe the term carcinoma should be applied to the tumor in his case and suggested that it be called carcinosis. Previous to this report, Dungal (4), who had been studying the condition in sheep, had reviewed the literature in a search for cases of adenomatosis in man and found instances reported by Helly (1907), Löhlein (1908), and Oberndorfer (1930). Of these, the one reported by Helly more closely resembled the condition described. In Oberndorfer's case, metastases were present; Löhlein's patient had a single apple-sized tumor in the lower lobe of the right lung. In 1943, Sims (9) reported a case which he classified as pulmonary adenomatosis (Case 1 in our series) and also stressed the resemblance to jaagsiekte. Copyrighted 1946 by The Radiological Society of North America, Inc.

Benign pulmonary adenomatosis is a disease with multiple involvement of the lungs by a process in which the alveoli are filled with mucus-filled columnar cells and extrapulmonary metastases do not occur. All reports in the American literature have appeared since 1939. This emphasizes the recent recognition of the condition in this country. Only in a few reports has the clinical picture been considered. This report records a case demonstrating certain features that when present may facilitate clinical recognition of pulmonary adenomatosis. REPORT OF CASE R. M., a 39 year old white male bookkeeper, was in good health until June 1947, when he had an acute illness manifested by pleuritic pain, chill, fever and cough productive of blood-streaked sputum. He entered a hospital and was treated for pneumonia. He recovered from the acute illness but had residual symptoms of weakness and cough productive of a small amount of white sputum. In

Pulmonary Adenomatosis A Report of Four Cases 1 J. Cash King , M.D. and David S. Carroll , M.D. Memphis, Tenn. ↵ 1 From the Department of Radiology, University of Tennessee College of Medicine, Memphis, Tenn. Presented at the Thirty-fifth Annual Meeting of the Radiological Society of North America, Cleveland, Ohio, Dec. 4–9, 1949. Excerpt In 1939 Bonne reported a peculiar disease of the lungs in a 39-year-old Chinese, in which there existed a diffuse process of epithelial proliferation throughout the pulmonary alveoli. The symptoms were dyspnea, productive cough, and weight loss; and the disease killed the patient, although invasive and destructive growth was not present. Bonne stressed the resemblance to jaagsiekte in sheep and called the disease carcinosis. Since that report, cases have been found and diagnosed more and more frequently, and because the roentgenologist is often the first to see the changes in the lung, it is appropriate that we devote more time to the study and consideration of this condition. In this report we shall discuss the present status of the disease and add 4 cases, 3 of which have microscopic confirmation. Pathology In benign pulmonary adenomatosis firm nodules, varying in size, are scattered throughout both lungs. Grossly, these nodules resemble areas of pneumonic consolidation. On cut section, they have the appearance of the gray hepatization stage of pneumonia, and a mucoid material can be expressed from the areas of involvement. The bronchi are filled with frothy, thin mucoid material, and areas of congestion and edema are present throughout the lungs. Terminally there is usually a considerable degree of pneumonic consolidation superimposed upon the adenomatosis. The pleura is usually not involved but may show areas of fibrinous or fibrous adhesions. In the typical case there are no metastases either in the regional lymph nodes or in distant organs. Microscopically, the process is much more extensive than one would suspect from the gross examination. The alveoli are lined by cuboidal and columnar epithelium, and in many areas there is overgrowth of the epithelium to form papillary extensions into the alveolar spaces. The alveolar lining cells are usually quite uniform in appearance and are non-ciliated. There are few or no mitotic figures. The alveolar septa are not invaded, and there is no extension into the interalveolar tissues. The walls of the alveoli are edematous, and there is a varying degree of fibrosis of the interstitial supportive tissues. Clinical Features Dyspnea is the most constant feature of pulmonary adenomatosis, increasing in severity throughout the course of the disease. This can readily be explained by the microscopic findings. The remarkable hyperplasia of the epithelium in the alveoli interferes to a great extent with the gaseous exchange between the alveoli and pulmonary capillaries. Furthermore, the accumulation of mucoid material in the bronchi interferes with the passage of air to the alveoli. Cough is also a constant and striking feature. In the early stages the cough is productive of very small quantities of thin, watery mucoid sputum, but as the disease progresses the cough increases in severity and production of 40 to 50 ounces of sputum in a twenty-four-hour period is common. Copyrighted 1950 by The Radiological Society of North America, Inc.