Classical scrapie is a transmissible spongiform encephalopathy that attacks the central nervous system of sheep and goats. Since its discovery in the 18th century, the disease has caused enormous economic losses and public health impacts in continental Europe. In the late 20th century, classical scrapie began to spread to places, such as Asia and the Americas, becoming a disease of global concern. In this study, based on prion occurrence records and high-resolution environmental layers, a risk assessment of classical scrapie in China was performed using a maximum entropy model. The model achieved an area under the curve value of 0.906 (95% confidence interval, 0.0883–0.0929). Sheep distribution density, road density, goat distribution density, minimum temperature of the coldest month, port density, and precipitation of the driest quarter were identified as important factors affecting the occurrence of classical scrapie. The risk map showed that potential high-risk areas in China were mainly located in Northeast China, North China, and Northwest China. This study can provide a valuable reference for the prevention of classical scrapie in China. According to the environmental variables and risk areas of classical scrapie, implementing monitoring and early warning measures in these areas is recommended to reduce the possibility of classical scrapie occurrence and transmission.

Pasteurella multocida can cause goat hemorrhagic sepsis and endemic pneumonia. Respiratory epithelial cells are the first line of defense in the lungs during P. multocida infection. These cells act as a mechanical barrier and activate immune response to protect against invading pathogenic microorganisms. Upon infection, P. multocida adheres to the cells and causes changes in cell morphology and transcriptome. ATAC-seq was conducted to determine the changes in the chromatin open region of P. multocida-infected goat bronchial epithelial cells based on transcriptional regulation. A total of 13,079 and 28,722 peaks were identified in the control (CK) and treatment (T) groups (P. multocida infection group), respectively. The peaks significantly increased after P. multocida infection. The specific peaks for the CK and T groups were annotated to 545 and 6632 genes, respectively. KEGG pathway enrichment analysis revealed that the specific peak-related genes in the T group were enriched in immune reaction-related pathways, such as Fc gamma R-mediated phagocytosis, MAPK signaling pathway, bacterial invasion of epithelial cells, endocytosis, and autophagy pathways. Other cellular component pathways were also enriched, including the regulation of actin cytoskeleton, adherent junction, tight junction, and focal adhesion. The differential peaks between the two groups were subsequently analyzed. Compared to those in the CK group, 863 and 11 peaks were upregulated and downregulated, respectively, after the P. multocida infection. Fifty-six known transcription factor motifs were revealed in upregulated peaks in the P. multocida-infected group. By integrating ATAC-seq and RNA-seq, some candidate genes (SETBP1, RASGEF1B, CREB5, IRF5, TNF, CD70) that might be involved in the goat bronchial epithelial cell immune reaction to P. multocida infection were identified. Overall, P. multocida infection changed the structure of the cell and caused chromatin open regions to be upregulated. In addition, P. multocida infection actively mobilized the host immune response with the inflammatory phenotype. The findings provide valuable information for understanding the regulatory mechanisms of P. multocida-infected goat bronchial epithelial cells.