Review For Ovine Pulmonary Adenomatosis(OPA)
Ovine pulmonary adenomatosis, also known as ovine pulmonary
carcinomatosis(OPC), is a contagious, highly transmissible,
retroviral induced bronchioloalveolar carcinoma of ovine
lungs. The disease is caused by a retrovirus which cannot
be cultivated in vitro. Morphologic, biochemical, and immunologic
findings proved that a type B/D-related retrovirus is the
etiologic agent.
The disease is transmitted by inhalation of infectious
droplets when sheep are kept in close contact. OPA usually
affects mature sheep between 1-4 years-of-age and disease
onset is insidious. The clinical manifestations include
progressive weight loss, exercise intolerance, tachypnea,
and dyspnea. Moist crackles are audible over the affected
areas and may be heard at a distance so that the affected
group of animals are said to produce a sound like slowly
boiling porridge. A diagnostic test for the disease is to
hold the sheep by the hindlegs while lowering the head.
In affected animals a quantity of copious, thin mucoid fluid
(up to 200 ml), presumably produced by the neoplastic cells
in the lung, pours from the nostrils. Appetite and rectal
temperature are usually normal. Sheep die within a few weeks
to six months after first exhibiting clinical signs from
complicating Pasteurellahemolvtica pneumonia.
The only reported laboratory abnormality in OPA
is hypergammaglobulinemia.
Early gross lesions are enlarged, heavy (two to three times
more than normal), and wet lungs which contain several firm,
gray or light purple, variably-sized nodules that are separated
from normal parenchyma by a narrow zone of emphysema. In
the later stage these nodules become confluent and large
segments of both lungs are diffusely but not symmetrically
infiltrated by neoplastic cells. On cross section, a copious
mucoid secretion is in the airways. Microscopically,
the nodules are composed of cuboidal or columnar epithelial
cells lining airways and alveoli and forming papillary ingrowths
in adenomatous (gland-like) patterns. These cells have been
identified ultrastructurally as originating from both the
type II alveolar epithelium (pneumocytes) and non-ciliated
bronchiolarepithelium (Clara cells). Nasal exudate or tracheal
wash fluid contains spherical clusters of epithelial cells
which have the hyperplasticadenomatous epithelium typical
of pulmonary lesions and increased numbers of macrophages.Sequelae
often include secondary bronchopneumonia, abscesses, and
fibrous pleural adhesion. Metastases to tracheobronchial
lymph nodes and to a lesser extent to other tissues such
as pleura, muscle, liver and kidney also occur.
Diagnosis of OPA should be based on the presence, in a
single mature sheep, of afebrile, wasting disease with marked
respiratory distress. No treatment is advised and any case
showing loss of weight and signs of respiratory disease
should be isolated and veterinary advice sought. Prompt
culling of any suspicious animals is advised.
References:
Lofstedt,J., Progressive viral pneumonia of sheep and goats.
In Smith BP,ed: Large Animal Internal Medicine, ed 2, St.
Louis, 1996, Mosby, pp 669-670.
Diseases caused by viruses and chlamydia-II. In RadostitisOM,
Blood DC, and Gay cc,ed:
Veterinary Medicine, ed 8, London,
1994, BailliereTindall, pp 1075-1077.
Sharp, JM, Chronic respiratory vims infections.
In Martin WB and Aitken,ed: Diseases of Sheep, ed 2, London,
1991, Blackwell Scientific Publications, pp 143-147.
Sharp, JM and Angus, KW, Sheep pulmonary adenomatosis:
clinical, pathological, and epide-miological aspect. In
Petursson,G. and Hoff-Jorgenson,R.,ed: Developments of Veterinary
Virology, Maedi-Visna and Related-Diseases, Boston,
1990, Kluwer Academic Publishers, pp 157-175.
- byHasanAtyani,ECFVG
- edited by KathyClarke,DVM
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