Pathogenesis and clinical pathology:

lamb (source 10).

      

The OPP virus persists within infected monocytes and macrophages and may exist in a latent state for an undetermined amount of time. Antigenic variation of the surface proteins of the virus facilitates its persistence in the host. Research has shown the virus to have a 2 to 4 yr incubation period, so clinical signs are usually seen in older ewes (source 1). The virus infects cells by attaching to cell surface receptors. Once inside the cell, the virus replicates its RNA genome using  a DNA intermediate provirus, which is integrated into the chromosomal DNA of infected cells, and thus the host can not eliminate the virus and is persistently infected. The immune response of the animal can restrict the viral replication process, however it fails to eliminate the virus completely. Some sheep may not develop an immune response until several months after infection (source 2).

The main mode of transmission is to the lamb via the colostrum. The chance of transmission via the milk increases with the period of contact between the dam and the neonate, but can occur within the first ten hours of life (source 2). Vertical transmission is possible, however it is rarely observed. Lateral transmission can occur in older sheep and is respiratory in nature, with close confinement of sheep being a confounding factor. Lateral transmission can contribute to rapid spread of OPPV within the flock.  Infection of ewes by semen contaminated with infected leukocytes is another means of lateral transmission. Blood has not been demonstrated to be a source of transmission (source 1). The outcome for an animal that became infected as a lamb is influenced by the viral phenotype, the infectious dose, passive transfer of immunity, the age of the animal, as well as the host’s genetic factors. Many sheep remain asymptomatic carriers for life. Other infected sheep are persistently viremic despite attempts at humoral protection.

The virus has a significant ability to mutate and antigenic drift produces new strains, each of which has different patterns of disease. In most cases, the pathology is localized in lungs, central nervous system, and in hematopoietic tissues. In the lung the virus stimulates reticular cells and lymphocytes to proliferate resulting in thickening of interalveolar septae, and adenomatosis of the alveoloar lining. Regional lymphadenopathy is common as well. Other pathological processes include indurative lymphocytic mastitis, proliferative arthritis and non-suppurative encephalitis, although this is seen less frequently. In the central nervous system, there is infiltration of the meninges and white matter with lymphocytes.  Demyelination occurs from the direct effect of the virus on oligodendrocytes and astrocytes as well as being the result of an inflammatory response to the cells containing viruses (source 2).