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Respiratory System
Respiratory Diseases of Sheep and Goats
Progressive Pneumonia in Sheep and Goats
Etiology and Pathogenesis
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Topics in Respiratory Diseases of Sheep and Goats
  • Overview of Respiratory Diseases of Sheep and Goats
  • Sheep Nose Bot
  • Contagious Caprine Pleuropneumonia
  • Pasteurella and Mannheimia Pneumonias in Sheep and Goats
  • Progressive Pneumonia in Sheep and Goats
  • Pulmonary Adenomatosis in Sheep and Goats
     
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    Progressive Pneumonia in Sheep and Goats(Maedi, Zwoegersiekte, La bouhite, Graaff-Reinet disease)

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    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 in paresis and 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). Finnish breeds may have a greater tendency to become infected than other sheep breeds.

    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. Sero-positive 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 (hardbag) may occur. In the encephalitic form (visna), ataxia, muscle tremors, or circling progresses to paresis and eventually to complete paralysis.

    Lesions

    Macroscopic lesions of progressive pneumonia are confined to the lungs and associated lymph nodes. The lungs do not collapse when the thorax is opened and are abnormally firm and heavy (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 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.

    Diagnosis

    Differential diagnoses of progressive pneumonia include pulmonary adenomatosis (jaagsiekte, see below), verminous pneumonia, and pulmonary caseous lymphadenitis. Necropsy with histopathologic examination of affected lung tissue is very useful in differentiating these various types of pneumonias. Listeriosis, scrapie, louping ill, rabies, 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 (AGID) and ELISA tests are available. AGID is highly specific (100%), with a sensitivity that ranges from 11% (2 wk after infection) to 100% (5 wk after infection). The competitive inhibition ELISA is reported to be highly sensitive and specific; it has been reported to produce false-negative results in animals that are very recently infected. Serologic testing is considered a useful tool in detecting 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 for detecting virus. However, both are more expensive and time consuming than serologic testing.

    Control

    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.

    Last full review/revision March 2012 by Michelle Kopcha, DVM, MS

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