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Ovine Pulmonary Adenocarcinoma

(Jaagsiekte, Sheep pulmonary adenomatosis)

By Philip R. Scott, BVM&S, MPhil, DVM&S, DSHP, DECBHM, FHEA, FRCVS, University of Edinburgh

Ovine pulmonary adenocarcinoma (OPA) is a contagious, viral, neoplastic disease of the lungs of sheep and more rarely of goats. It has been reported from Europe, Asia, Africa, and South and North America.

Etiology:

OPA is an infectious neoplastic lung disease resulting from infection with a beta retrovirus called Jaagsiekte sheep retrovirus (JSRV). The virus replicates predominantly in the tumor cells, is released into the airways, and is found in respiratory secretions. Transmission of JSRV occurs predominantly through the aerosol route by inhalation of infected respiratory secretions, although the virus may also be transmitted via colostrum and milk.

Clinical Findings:

The period of incubation after natural infection extends over months, so clinical signs generally become evident when sheep are 2–4 yr old. However, disease may be seen in lambs 8–12 mo old that are progeny of infected dams. The tumors produce clinical signs when they become sufficiently large or numerous enough to interfere with respiration. Affected sheep lose weight and show increasing respiratory distress and panting. Crackles are audible over a much larger area than the distribution of OPA lesions determined ultrasonographically. Coughing is not prominent, and infected animals are afebrile unless secondary infection develops. During the advanced stages of clinical disease, the tumor mass may occupy up to 60% of lung parenchyma. Clinical disease ends in death after many months but sometimes within 1–2 days due to secondary pasteurellosis.

Lesions:

Tumors are confined to the lungs and, rarely, the associated lymph nodes. They vary from small nodules to extensive solid areas that involve the ventral parts of one or more lobes and are firm, gray, flat, and sharply demarcated. Copious amounts of white, frothy fluid are present in the air passages. Histologic changes are caused by uncontrolled proliferation of columnar-shaped type II pneumonocytes and similar cells in the bronchioles (Clara cells).

Diagnosis:

Chronic weight loss, dyspnea, crackles, and copious amounts of serous nasal discharge from accumulated lung fluid in an adult sheep that is afebrile are highly suggestive clinical signs of OPA.

During the advanced stages of clinical disease, several mL of a clear, frothy fluid may flow freely from both nostrils when the sheep’s head is lowered during feeding; this quantity may exceed 50 mL if the hindquarters are raised when the head is simultaneously lowered (colloquially referred to as the “wheelbarrow test”). This test causes affected sheep considerable distress and must be discontinued as soon as some clear fluid appears at the nostrils; euthanasia is warranted immediately once this positive result is obtained. Not all cases of OPA produce this fluid in detectable amounts even in the advanced stages of disease. Therefore, a negative wheelbarrow test should not be considered conclusive, although a positive wheelbarrow test is pathognomonic for OPA.

There is presently no commercial confirmatory serologic test for OPA. The PCR test has been used in research on OPA for several years. However, whereas the test is highly sensitive in laboratory assays, it fails to detect JSRV in most infected sheep other than overt clinical cases. This is because there are few infected cells in the blood during the early stages of disease progression. Bronchoalveolar lavage has been used on sedated sheep to collect cells from the airways, followed by DNA extraction and PCR testing. Although this method appears to offer better sensitivity than the blood test, the sample collection method does not lend itself to routine on-farm large-scale testing.

Ultrasonography can be used to differentiate chronic lung pathologies and support a diagnosis of OPA, including superficial lung lesions as small as 1–2 cm in diameter. The first indication of changes in the superficial lung parenchyma caused by OPA is the abrupt loss of the bright linear echo formed by normal aerated lung tissue (visceral or pulmonary pleura) to be replaced by a hypoechoic area in the ventral margins of the lung lobes at the fifth or sixth intercostal spaces.

Control:

No specific treatment or vaccine is available. Affected sheep must be culled as soon as clinical suspicions are confirmed by ultrasonographic examination of the chest. Antibiotic therapy may temporarily improve the clinical appearance of those sheep with significant secondary bacterial infection. Good biosecurity is essential to minimize the risks of introducing OPA to unaffected farms with purchased sheep. At this time, the best that can be recommended once a diagnosis is confirmed is removal of all animals showing signs suggestive of pulmonary adenomatosis. However, subclinically infected sheep serve as a reservoir for the virus. Maintaining sheep in single-age groups is the most important management factor to reduce clinical disease.

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