Mycobacterium avium subspecies paratuberculosis (MAP) causes chronic, wasting, and progressive enteritis in cattle, bringing significant economic losses in livestock industries. MAP has spread worldwide mainly due to movement of animals. The objective of this study was to determine the MAP seroprevalence in cattle in the Xinjiang Uygur Autonomous Region, Northwest China, and evaluate the difference between intensive farming herds (cattle number in a herd is more than 200, and the cattle cannot have access to pasture) and free-range herds (the cattle are bred by individual households, a herd is defined as the cattle are bred in a village or town in this study). A total of 3157 serum specimens were collected from 42 herds in nine different regions. This included 1481 specimens from 18 intensive farming herds in four regions and 1676 specimens from 24 free-range herds in six regions. Antibody against MAP was tested with commercial ELISA test kits. The results showed that the overall apparent prevalence was 4.8% (95% CI, 4.1 to 5.6%) at animal level, and 50.0% (21/42) at herd level. The apparent prevalence in intensive farming herds and free-range herds were 9.5% (141/1481) and 0.7% (11/1676) at the animal-level, 88.9%(16/18) and 20.8% (5/24) at herd level, respectively, with a significant statistical difference between these two farming modes (p < 0.01). Cattle in intensive farming herds had a relatively higher risk to be infected with MAP than those in free-range herds (RR = 14.4). This study demonstrates that apparent prevalence of MAP infection in dairy cattle differs with farming modes at the animal level and herd level, and farming density could be an important risk factor associated with the presence of MAP infected cattle. This study provides important epidemiological data for bovine MAP control in Xinjiang, Northwest China.

To date, cases of snake infection caused by Morganella morganii and its effects on the intestinal microecology of snakes remain poorly documented. A pathogenic strain, designated NM-11, was isolated from diseased and dead snakes collected from a snake farm in China. In this study, strain NM-11 was identified as Morganella morganii through morphological observation, physiological and biochemical characterization, 16S rRNA gene sequencing, as well as genome-based average nucleotide identity (ANI) and digital DNA–DNA hybridization (dDDH) analyses. Subsequently, artificial challenge assays were performed to evaluate its pathogenicity. The whole genome of the strain was sequenced using PacBio long-read technology, and antimicrobial susceptibility tests were conducted to characterize its antibiotic resistance profile. Furthermore, high-throughput sequencing was applied to explore the alterations in intestinal microbial diversity of Ptyas mucosus upon infection with strain NM-11. Pathogenicity assays revealed that strain NM-11 exhibited strong virulence. After experimental infection, Ptyas mucosus displayed typical clinical signs including depression, lethargy and diarrhea. Gross pathological examination revealed extensive hemorrhage in the abdominal cavity, lungs and gastrointestinal tract, and histopathological observation confirmed severe lesions in multiple organs. Antimicrobial susceptibility tests confirmed the strain was multidrug-resistant (MDR). It had high resistance to many antibiotics. These drugs include polymyxin B, tetracycline, cefuroxime, cephalexin, erythromycin, vancomycin and streptomycin. Intestinal microbiota analysis indicated that infection with NM-11 remarkably reshaped the intestinal microbial community structure of Ptyas mucosus and increased the overall microbial diversity, accompanied by a significant rise in the relative abundance of Morganella morganii . This is the first report of Morganella morganii isolated and identified from diseased snakes in China. Our findings clarify the pathogenic characteristics and antibiotic resistance profile of this resistant strain against Ptyas mucosus . The results provide fundamental scientific evidence for the clinical diagnosis and antimicrobial prevention and treatment of Morganella morganii infection in snakes, and also offer valuable insights for reptile medicine and public health risk prevention and control.

Heat stress (HS) causes reproductive damage in female mammals, including pigs, cattle, and sheep. As the primary site of estrogen (E₂) biosynthesis, follicular granulosa cells (GCs) act as the critical target of HS injury. Previous studies have shown that cinnamaldehyde (CA) effectively participates in reproductive regulation in mice. Therefore, female mice and their follicular GCs were taken as the research subjects in this study. First, we adopted ELISA and H&E staining to investigate the effects of CA on ovarian follicular histology and E₂ secretion in mice. Second, CCK-8 assay, flow cytometry, and ELISA were applied to clarify how CA regulates proliferation, apoptosis, and E₂ secretion of mouse follicular GCs under HS. Finally, RT-qPCR and Western blotting (WB) were used to elucidate the protective effects of CA together with its underlying molecular mechanisms. Animal experiment results revealed that HS elevated the proportion of primordial and primary follicles and suppressed E₂ secretion. Oral gavage of mice with CA at 25 mg/kg exhibited no obvious hepatotoxicity. This dosage effectively increased the percentage of secondary and antral follicles, alleviated HS-induced histological damage in ovaries, and raised serum E₂ levels both under normal conditions and HS. Further in vitro cell experiments confirmed that HS reduced cell viability and accelerated apoptosis in mouse follicular GCs. HS decreased estrogen secretion by downregulating the relative protein expression of StAR and CYP19A1. Treatment with CA at a concentration of 2.5 × 10⁻⁵ M significantly increased cell viability and inhibited excessive apoptosis in mouse follicular GCs under HS. Under HS conditions, CA treatment elevated E₂ secretion in mouse follicular GCs by upregulating the relative protein expression of StAR and CYP19A1. In conclusion, the findings of this study indicate that CA holds promise as a natural anti-HS additive.