Veterinary pathology · 2025
Cerebellar hypomyelination, white matter vacuolization, and prolonged presence of atypical porcine pestivirus in pigs with congenital tremor type A-II.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Bergfeldt Anna, Myrmel Mette, Ranheim Birgit, Aae Frida, Sørby Randi
Аннотация
Atypical porcine pestivirus (APPV) is responsible for congenital tremor (CT) type A-II in pigs, a globally distributed neurological disease, with many unresolved questions regarding its pathogenesis and pathology. This descriptive case-control study assessed the viral load of APPV and its association with lesions in the central nervous system (CNS), as piglets born with severe clinical signs of CT recovered from clinical disease. The virus was found in all pigs with CT across 3 age groups (newborn, 3-week-old, 4- to 5-month-old CT pigs) using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The highest viral load was observed in the spinal cord of newborns and in the cerebellum of older groups. No APPV was detected in control pigs. Histologic evaluation revealed variable vacuolization in the CNS white matter of CT-affected pigs, which was most prominent in the spinal cord, cerebellum, and cerebrum of newborns, and in the cerebellum and cerebrum of 3-week-old pigs. Transmission electron microscopy demonstrated hypomyelination in newborn and 3-week-old CT pigs, but myelin levels comparable to those of control pigs in 4- to 5-month-old CT pigs. This research demonstrates the prolonged presence of APPV in the CNS of pigs born with severe signs of CT. Variable white matter vacuolization and hypomyelination can be found up to 3 weeks of age, but myelin levels normalize in older pigs, suggesting a delayed myelination process. Further research is needed to confirm the primary cellular target for APPV in the CNS and to understand how the virus affects the myelination process.