Isolation of a virus from the lungs of montana sheep affected with progressive pneumonia

VIROLOGY

36, 483-484 (1968)

ANNOUNCEMENT Isolation

of a Virus

from with

It.

C. KENNEDY,

the

Lungs

Progressive

C. 114. EKLUND,

of Montana

Sheep

Affected

Pneumonia

CARLOS

LOPEZ,’

AND

W. J. HADLOW

U.S. Department of Health, Education and Welfare, Public Health Service, National Institutes Kational Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratory, Hamilton, Montana, 59840

of Health,

In 1923, Marsh (1) described a chronic pulmonary disease of sheep in Montana. He called it progressive pneumonia. Mainly affecting older ewes, the disease is made manifest by slowly progressive loss of weight’, increasingly severe respiratory distress, and death after a course of 3-12 or more months. Histologically, it is characterized by widespread nodular proliferation of lymphocytes in the lungs and by pronounced thickening of interalveolar septa by lymphoreticular cells. Classification of this disease is uncertain, but some of its features are suggestive of lymphoma. Diseases closely resembling progressive pneumonia were later described in sheep in South Africa (a), France (3), The Netherlands (4), and Iceland (5). In 1936, Creech and Gochenour (6) reported experimental transmission of progressive pneumonia by the intrapulmonary or intravenous inoculation of sheep with a suspension of lung and mediastinal lymph nodes from naturally affected Montana sheep. Transmission of the disease by the intravenous inoculation of suspensions of lung from affected Mont’ana sheep was reported also by Duran-Reynals et al. (7) in 1958. During a personal conversation, Dr. Marsh mentioned he had produced t’he disease in a sheep inoculated with a Seitz filtrate of a suspension of affected lung. In 1953, Sigurdsson, PAlsson, and Tryggvadbttir (8) reported transmission of maedi, the strikingly similar pulmonary disease of Icelandic sheep. This was achieved by the combined intravenous, intrapulmonary, and intranasal inoculation of lambs with a suspension of lung from affected sheep. Sigurdarddttir and Thormar (9) stated that Sigurdsson, using a continuous tissue culture cell line derived from the choroid plexus of sheep, had isolated a virus in 1958 from explants and suspensions of maedi-affected lungs. T,ater, more isolations of this virus were made in t,issue cult’ure (9). It causes t’he formation of polykaryocytes in tissue culture, is about SO rnp in diameter, is rapidly inactivated at 56”C, and is sensitive to ether (10). When tissue culture virus was inoculated by several routes into sheep, it produced typical maedi (11) . In our laboratory, 10% suspensions of lungs from seven of seven sheep affected with either natural or experiment’al progressive pneumonia have produced, within 14 days, characteristic mult’inucleated giant cells, or polykaryocytes, in tissue culture cell lines derived from lungs of normal sheep and goats (Fig. 1). The agent can be readily maintained in serial passage. To date, the maximum IDso titer obtained in tissue culture has been 10-s.67. The agent passes through a Millipore filter of 220 rnp average pore diameter, but, is retained by one of 100 rnp average pore diameter. Exposure of a suspension of the virus containing 105.67TCID,, per 0.2 ml to 56°C for 10 minutes, or to diethyl ether for 20 hours at 4”C, 1 Graduate

st’udent,

Uuiversity

of Minnesota,

Minneapolis. 483

484

KENNEDY.

ET AL.

FIG. 1. Characteristic appearance of a cell monolayer 7 days after it was inoculated with the virus isolated from lungs of sheep affected with progressive pneumonia. Hematoxylin and eosin. X140.

completely inactivates it. These properties of the virus indieate it must be closely related to maedi virus . Because of this resemblance to maedi virus, and because it was isolated from all of seven affected sheep and from a 220-rnp Millipore filtrate of affected lung that caused typical progressive pneumonia in sheep, the virus described here is presumed to be the etiologic agent of the disease in Montana sheep. Experiments to determine whether this is so are in progress. REFERENCES 1.

H., J. Am. Vet. Med. Assoc. 15, 458-473 (1923). Union 8. Africa Dir. Bet. Serv. 16th Ann. Rept., 1929, pp. 611-641. LUCAM, F., Rec. Med. Vet. Ecole Alfort 118, 273-284 (1942). KOENS, H., “11e ‘zwoegers’ op Texel.” Thesis, Univ. of Utrecht, 1943. SIGURDSSON, B., GRIMSSON, H., and P~LSSON, P. A., J. Znfect. Diseases 90, 223-241 (1952). CREECH, G. T., and GOCHENOUR, W. S., J. Agr. Res. 52, 667-679 (1936). DURBN-REYNALS, F., JUNGHERR, E., CUB~-C.~P~R~, A., RAFFERTY, K. A., JR., and HELMBOLDT, C., Ann. N. Y. Acad. Sci. 70, 726-742 (1958). SIGURDSSON, B., P~LSSON, P. A., and TI~YGGVBD~TTIR, ANNA, J. Znfect. Diseases 93, 166-175 (1953). SIGURD~RD~TTIR, BERGTH~RA, and THORM~R, H., J. Infect. Diseases 114, 55-60 (1964). THORMAR, H., Proceedings of the International Conference on Lung Tumours in Animals, Stab. Tip. “Grafia” di Salvi & C., Perugia, It,aly, 1965, pp. 393-402, 1966. GUDND~TTIR, MARGRET, and P~LSSON, P. A., J. Infect. Diseases 117, 1-6 (1967). MARSH,

2. DEKOCK, G.,

3. 4. 6. 6. 7. 8. 9. 10. 11.