Ovine Progressive Pneumonia (OPP) is a chronic, slow-developing viral disease affecting sheep flocks worldwide. Caused by a lentivirus, OPP establishes a persistent, lifelong infection in affected animals. This infection leads to debilitating symptoms that progressively worsen over time. Outside the United States, the disease is often recognized as Maedi-Visna (MV), with the Icelandic names describing the primary forms of the illness. Since no cure exists, understanding how OPP develops and how to detect it accurately is essential for maintaining flock health and productivity.
The Causative Agent and Transmission Routes
The agent responsible for this infection is the Ovine Progressive Pneumonia Virus (OPPV), which belongs to the group of Small Ruminant Lentiviruses (SRLVs). OPPV is closely related to the virus that causes Caprine Arthritis-Encephalitis (CAE) in goats. As a lentivirus, OPPV integrates its genetic material into the DNA of the host cell, forming a provirus. This integration ensures the virus is replicated every time the host cell divides.
The main method of spread is the ingestion of infected colostrum or milk, the primary route of transmission from ewe to lamb. Horizontal spread between adult sheep is also common, occurring through the inhalation of aerosolized respiratory secretions. This transmission is most efficient when sheep are kept in close confinement, such as during winter housing or in crowded handling facilities.
Transmission can also occur via iatrogenic means, though less frequently, such as through the reuse of contaminated needles or equipment during flock management. Once the virus enters the body, it targets specific immune cells, which carry the infection throughout the animal. Infected sheep remain carriers for life and shed the virus continuously, even if they show no outward signs of illness.
Insidious Progression of the Disease
The slow progression of OPP results from its selective targeting of the host’s immune cells, specifically monocytes and macrophages. The virus uses these white blood cells as a reservoir to replicate and spread throughout the body. By hiding its provirus within the DNA of these cells, the virus evades the host’s immune response, leading to persistent antibody production that cannot clear the infection.
The resulting pathology is characterized by a chronic inflammatory response. Infected macrophages and circulating lymphocytes accumulate in specific organs, causing a dense infiltration of mononuclear cells. Over years, this cellular infiltration gradually replaces healthy, functional tissue, leading to tissue hardening and organ dysfunction.
In the lungs, chronic inflammation manifests as lymphocytic interstitial pneumonia, known as Maedi. The connective tissue between the airways thickens, making the lungs heavy and firm. This cellular infiltration impairs oxygen exchange. The inflammation also commonly affects the udder, leading to indurative mastitis or “hard bag,” where milk-producing tissue is replaced by hardened, non-functional lymphoid tissue.
The disease can also target the joints, resulting in arthritis. Less commonly, particularly in North American strains, OPP affects the central nervous system, causing neurological signs known as the Visna form of the disease.
Recognizing Clinical Manifestations
The slow, progressive nature of OPP means clinical signs rarely appear in sheep younger than four years old, although initial infection occurs much earlier. The symptoms that emerge are a consequence of long-term inflammatory damage to multiple organ systems. A common initial sign is a gradual loss of body condition, often termed “thin ewe syndrome,” where the animal wastes away despite maintaining a normal appetite.
As lung damage progresses, sheep show increased respiratory effort, especially after exercise, and may breathe rapidly or with an open mouth. These animals, sometimes called “lungers,” lag behind the flock and become highly susceptible to secondary bacterial pneumonias. When the mammary gland is affected, the udder becomes firm and enlarged but produces little to no milk. This condition is not painful or hot like bacterial mastitis.
Joint involvement typically presents as lameness or swollen carpal joints, causing a stiff or shortened gait. The cumulative effect of these manifestations leads to significant economic loss. This loss results from premature culling, reduced lamb weaning weights due to poor milk supply, and lower flock productivity.
Interpreting Diagnostic Results
Because clinical signs appear late, OPP detection relies heavily on diagnostic testing to identify asymptomatic carriers. The most widely used method involves serology, which detects the presence of antibodies against the virus in the animal’s blood. The two common serological tests are the Agar Gel Immunodiffusion (AGID) test and various Enzyme-Linked Immunosorbent Assays (ELISA).
ELISA is generally considered more sensitive, capable of detecting antibodies earlier than the AGID test. A major challenge in serological testing is the “window period,” the time between initial infection and the production of detectable antibodies, which can take several weeks to months.
Furthermore, lambs nursing from infected ewes may test positive due to the passive transfer of maternal antibodies. This result is inconclusive until the lamb is retested after six months of age.
Molecular methods, such as Polymerase Chain Reaction (PCR), directly detect the viral DNA (provirus) integrated within the host’s white blood cells. PCR is particularly useful for testing young lambs before they are expected to seroconvert or for confirming infection in animals with questionable serological results. However, PCR is significantly more expensive and is not typically used for large-scale flock screening.
The long incubation period and viral latency mean that a single negative test result does not guarantee an animal is free of infection, especially in young stock or recently exposed adults. For this reason, effective control programs rely on repeated, regular testing, often annually or semi-annually, to catch animals that seroconvert later. Producers implement a “test-and-cull” strategy, removing all positive reactors to eliminate the virus from the flock and prevent further transmission.