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Progressive Pneumonia in Sheep and Goats

(Maedi, Zwoegersiekte, La bouhite, Graaff-Reinet disease)

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

Ovine progressive pneumonia and maedi-visna are chronic diseases of sheep caused by lentiviruses (family Retroviridae) that are structurally and antigenically similar. Progressive pneumonia virus and maedi (meaning “dyspnea”) virus induce chronic progressive pneumonias that present with similar clinical signs. Visna (meaning “wasting”) is the term used in many parts of the world to refer to the neurologic form of the disease in sheep, resulting initially in unilateral pelvic paresis, progressing to paralysis. A closely related lentivirus-induced disease in goats, caprine arthritis and encephalitis (CAE, see Caprine Arthritis and Encephalitis), affects the nervous system and joints. Reported seroprevalence for lentiviral infection in sheep varies widely, ranging from 49% in the western USA to 9% in the north Atlantic region. This variation has been reported in other countries as well and may result from varied climatic conditions (arid vs more lush climates) and management (range conditions vs close confinement).

Etiology and Pathogenesis:

The causal lentivirus, which persists in lymphocytes, monocytes, and macrophages of infected sheep in the presence of a humoral and cell-mediated immune response, can be detected by several serologic tests. Seropositive sheep and goats must be considered infected and capable of transmitting the virus. Transmission occurs most commonly via the oral route, usually by ingestion of colostrum or milk that contains virus, or by inhalation of infected aerosol droplets. Intrauterine infection is thought to occur infrequently. All breeds of sheep and goats appear susceptible; however, some resistance to lentivirus infection may exist within breeds. Management practices can influence morbidity rates.

Clinical Findings:

Signs rarely occur in sheep <2 yr old and are most common in sheep >4 yr old. The disease progresses slowly, with wasting and increasing respiratory distress as the main signs. Coughing, bronchial exudate, depression, and fever are seldom evident unless secondary bacterial infection occurs. A noninflammatory, indurative mastitis may occur. The encephalitic form of visna causes head tilt and circling, whereas the spinal form causes unilateral pelvic limb proprioceptive deficits progressing to paresis and eventually to complete paralysis.


Macroscopic lesions of progressive pneumonia are confined to the lungs and associated lymph nodes. The lungs do not collapse when the thorax (with obvious rib indentations) is opened and are abnormally firm and heavy (~2 kg; 2–4 times normal weight). Early lung changes may be difficult to detect, but later in the disease, lungs are mottled by gray and brown areas of consolidation. The mediastinal and tracheobronchial lymph nodes are greatly enlarged and edematous. Interstitial pneumonia, perivascular and peribronchial lymphoid hyperplasia, and hypertrophy of smooth muscle are seen throughout the entire lung. CNS lesions, when they occur, are those of meningoleukoencephalitis with secondary demyelination. All lesions are progressive and result from the cellular immune response of the host, and not directly from viral damage.


Differential diagnoses of progressive pneumonia include pulmonary adenocarcinoma, pleural abscesses, and pulmonary caseous lymphadenitis. Ultrasonographic examination is very useful to differentiate these various types of pneumonias in the live animal. Listeriosis, scrapie, cerebrospinal nematodiasis, and space-occupying lesions should be considered when the neurologic form (visna) of the disease is seen.

In the live animal, agar gel immunodiffusion and ELISA tests are used. The competitive inhibition ELISA is reported to be highly sensitive and specific; it has been reported to produce false-negative results in animals very recently infected. Serologic testing is considered a useful tool to detect infected sheep, especially if the disease has been confirmed in the flock by histopathologic examination or virus isolation. PCR and virus isolation are sensitive and specific techniques to detect virus. However, both are more expensive and time consuming than serologic testing.


Currently, there is no practical, effective treatment, and no vaccines are available. Therefore, the only means for control and prevention is serologic testing and removal of positive animals. Because of the long incubation period and time to seroconversion, retesting animals once a year, or even twice a year, is recommended. In addition to the test and cull approach, consideration should be given to raising neonates in isolation from their dams, especially if the dam is seropositive. Lambs should be fed colostrum from seronegative sheep, or heat-treated sheep colostrum, and raised on milk replacer, milk from seronegative ewes, or heat-treated sheep milk.