Neuropathologic Study of Experimental Classical Swine Fever

Abstract

The aim of this study was to report on the lesions occurring in the central nervous system (CNS) during experimental classical swine fever (CSF) to clarify the spatial and chronologic distribution of the lesions and virus antigen in the CNS. To learn more about the pathogenetic mechanisms of the lesions during CSF in the CNS and to investigate the role of the virus in these mechanisms, cellular infiltrates and infected cells have been characterized. Twenty-eight pigs were inoculated with the virulent CSF virus isolate Alfort 187 and slaughtered from 2 to 15 postinoculation days; 4 animals of similar background served as a control group. Immunohistochemistry, electron microscopy, and the transferase-mediated deoxyuridine triphosphate nick-end labeling method were used to detect viral antigens and apoptosis. The results showed the presence of nonpurulent meningoencephalitis, occasional microhemorrhages, and apoptosis of the lymphocytes forming the perivascular and interstitital infiltrate in swine with CSF. Macrophages appeared to display little involvement in CNS lesions. The infected cells observed at the early stage of disease were lymphocytes and microglial cells in the rostral portion of the telencephalon, with infection of these cells in other areas in the next stages. The relationship between these lesions and the presence of viral antigen varied according to the type of lesion: hemorrhages were not associated with the presence of antigen in endothelial cells, but infiltrate-cell apoptosis was temporally and spacially associated to viral infection. However, the link between viral infection and the presence of cell infiltrate was far from clear.

Comparative studies on the pathogenicity and tissue distribution of three virulence variants of classical swine fever virus, two field isolates and one vaccine strain, with special regard to immunohistochemical investigations

“…It is noteworthy, that nervous tissue showed both histopathological lesions and the presence of viral antigen in Experiment I, while in Experiment II in spite of severe histopathological changes, CSFV antigen was not detected. To explain this peculiar phenomenon, one can speculate that: i) early cell damage may occur already at initial stage of viral replication, when the viral load is still low; ii) immune-mediated reactions may play role [ 16 ]. Concerning group III, the results of IHC indicated some virus replication between PIDs 5 and 8 in the tonsils and in the lymph nodes, but similarly to VI, only in three animals.…”

Classical Swine Fever—An Updated Review

“…In the acute course of CSF, pathology often reveals enlarged lymph nodes, hemorrhages and petechiae on serosal and mucosal surfaces of different organs such as the, lungs, kidneys, intestines and urinary bladder. Tonsillitis, necrotic ulcers in the intestines, lesions in the lymphoreticular system, and non-purulent encephalitis can be observed [126] Splenic infarctions can occur and are considered pathognomic for CSF [127]. Infected piglets develop leukopenia, thrombocytopenia and immunosuppression, which increases the risk for secondary infections and thus to diseases of the gastrointestinal and respiratory system [128].…”

Pulmonary intravascular macrophages regulate the pathogenetic mechanisms of pulmonary lesions during acute courses of classical swine fever

“…In the present study, numerical increase in PIMs was not accompanied by an increased rate in cell mitosis phenomena or less differentiated cells, so that alveolar septal thickening and hypercellularity might be attributed to the recruitment of peripheral blood mononuclear cells (PBMC). A significant decrease in PBMC, probably linked to cellular recruitment, together with inflammatory lesions and a significant increase in macrophages in different organs (thymus, intestine, liver, central nervous system) has been previously described at initial stages of infection with CSFV Alfort/187 strain (Gómez‐Villamandos et al., ; Núñez et al., ; Sánchez‐Cordón et al., , ). In parallel with the significant increase in pulmonary macrophages, there was an increase in infected PIMs.…”