Fermented traditional Chinese medicines (TCMs) have been identified as a low-cost and promising feed additive to to alleviate weaning stress in young livestock and poultry effectively. This study investigated the impact of probiotic fermentation on the metabolite content of BanQi (Radix Isatidis and Astragalus membranaceus) extract while also examined the effects of both fermented-BanQi (FBQ) and unfermented-BanQi (UBQ) on growth performance, serum biochemistry, intestinal villi, and gut microbiota in weaned lambs. This study demonstrated that compared with UBQ, FBQ contained significantly higher levels of free amino acids (e.g., phenylalanine and isoleucine), short peptides (e.g., Val–Leu–Pro–Val–Pro–Gln and Gly–Leu), and the active ingredients (e.g., vindesine and reserpine) (P < 0.05). The addition of FBQ to the diet significantly increased the final body weight and average daily gain of weaned lambs (P < 0.05). In addition, FBQ significantly increased the total protein level in the serum and the villus length of the jejunum and ileum in lambs, while significantly reduced the levels of aspartate aminotransferase (AST) and urea (P < 0.05). Sequencing of the intestinal flora showed that FBQ improved the diversity of intestinal flora and promoted the enrichment of beneficial bacteria in the lamb intestine, such as Mogibacterium and Butyrivibrio, compared to NC or UBQ groups (P < 0.05). Fermentation with Bacillus subtilis can enhance the content of free amino acids, peptides, and active ingredients in BanQi extract, making it an effective method to improve the efficacy of traditional Chinese medicine. Adding FBQ to the diet can improve the growth performance of weaned lambs, and its mechanism may be related to increasing the height of intestinal villi and increasing the diversity of intestinal flora.

Goose gout, a metabolic disorder characterized by systemic urate deposition in visceral organs (e.g., liver, kidneys) and joints of goslings, is strongly associated with goose astrovirus (GAstV) infection and environmental stressors such as high humidity. This disease severely compromises growth performance and survival rates, yet no licensed prophylactic or therapeuti interventions are currently available. Here, we investigated the efficacy of SIA, a Chinese herbal formula comprising Saposhnikovia divaricata, Isatis indigotica and Astragalus membranaceus against GAstV-induced gout in goslings. An experimental model was established by combining oral GAstV challenge with high-humidity environmental exposure. We systematically evaluated the protective effects of SIA by monitoring mortality rates, growth parameters (body weight, feed conversion ratio), serum biomarkers (uric acid, creatinine, inflammatory cytokines), and histopathological alterations in target organs. Furthermore, 16S rRNA sequencing was employed to analyze shifts in intestinal microbiota composition. Notably, medium-dose SIA administration significantly reduced mortality (p<0.05), restored growth performance, and attenuated hepatic and renal pathologies. Serum analysis revealed marked decreases in serum uric acid and creatinine levels, alongside suppression of pro-inflammatory cytokines. Mechanistically, SIA treatment modulated gut dysbiosis by reducing the relative abundances of pathogenic taxa, including Oceanobacillus picturae, Veillonellales, Streptococcus equinus and Synechococcus while promoting commensal microbiota associated with intestinal homeostasis.These findings highlight the dual prophylactic and therapeutic potential of SIA against goose gout, likely mediated through multi-target mechanisms involving renal urate excretion, anti-inflammatory activity, and gut microbiota regulation. This study provides a scientific foundation for developing SIA as a phytotherapeutic agent for goose gout management.

Porcine reproductive and respiratory syndrome is endemic worldwide, seriously affecting development of the pig industry, but vaccine strategies have limited protective effects against PRRSV transmission. The aim of this study was to identify potential anti-PRRSV drugs. We examined the cytotoxicity of seven compounds formulated by the mass ratio between glycyrrhizic acid and matrine and their inhibition rate against PRRSV in vitro. The results showed that the seven compounds all had direct killing and therapeutic effects on PRRSV, and the compounds inhibited PRRSV replication in a time- and dose-dependent manner. Then, the compound with the best anti-PRRSV effect was selected for subsequent in vivo experiments. Pigs were divided into a control group and a medication group to conduct the in vivo evaluation. The results showed that pigs treated with the 4:1 compound had 100% morbidity after PRRSV challenge, and the mortality rate reached 75% on the 8th day of the challenge. These results suggest that this compound has no practical anti-PRRSV effect in vivo and can instead accelerate the death of infected pigs. Next, we further analyzed the semiprotective pigs obtained from the vaccine through the compound to determine whether the compound can synergize with the vaccine in vivo. The results indicated that pigs treated with the compound had higher mortality and more severe clinical reactions after PRRSV infection (p < 0.05). The levels of proinflammatory cytokines (IL-6, IL-8, IL-1β, IFN-γ, TNF-α) were significantly upregulated in the compound-treated pigs compared to the positive control group (p < 0.05), and there was no synergistic enhancement with the live attenuated PRRSV vaccine (p < 0.05). The compound enhanced the inflammatory response, prompted the body to produce excessive inflammatory cytokines and caused body damage, preventing the therapeutic effect from being produced. In conclusion, the present study revealed that effectiveness in vitro does not mean that it is effective in vivo in developing anti-PRRSV drugs. Our finding showed that, in order to find the effective anti-PRRSV drugs, comprehensive drug screening is required, at least with solid anti-inflammatory ability in vitro and in vivo. Our study may help the development of new anti-PRRSV drugs.

Goose astrovirus-2 (GAstV-2) is the major etiological agent responsible for hyperuricemia and visceral gout in goslings, which causes substantial economic losses to the goose-raising industry. However, the complete pathogenic mechanisms underlying GAstV-2-induced hyperuricemia have not been fully elucidated. In this study, 1-day-old healthy Yangzhou goslings were orally inoculated with GAstV-2 to establish a viral infection model. The effects of GAstV-2 infection on growth performance, serum uric acid levels, cecal microbiota structure, and renal gene expression of goslings were systematically investigated. The results showed that GAstV-2 infection caused a cumulative mortality rate of 10%-30% in goslings and significantly impaired growth performance, as reflected by decreased average daily gain and average daily feed intake as well as an increased feed-to-gain ratio (P < 0.05). In addition, GAstV-2 challenge induced severe histopathological damage to the liver and kidney, disordered serum biochemical metabolism, and excessive release of pro-inflammatory cytokines, accompanied by a significant elevation in serum uric acid levels (P < 0.05). The 16S rRNA high‑throughput sequencing results confirmed that GAstV‑2 infection significantly decreased the abundances of uric acid‑degrading beneficial bacteria, including Paenibacillus polymyxa, Oscillospira guilliermondii, and Lactococcus lactis, while markedly increasing the abundance of Clostridium perfringens, which is closely associated with uric acid synthesis. Renal transcriptomic analysis confirmed that key genes involved in purine metabolism, including PRPS, IMPDH1, and NT5E, were significantly upregulated in the kidney tissues of infected goslings, which was closely correlated with the occurrence of hyperuricemia. In conclusion, GAstV-2 infection markedly inhibits growth, triggers hepatic and renal injury, increases serum uric acid and inflammatory levels, and remodels the intestinal microbiota composition and renal transcriptomic profiles in goslings. This study systematically explored the influences of GAstV-2 infection on growth performance, hepatorenal injury, and serum uric acid metabolism in goslings, and preliminarily revealed the potential underlying mechanism of GAstV-2-induced hyperuricemia by separately analyzing intestinal microbiome and renal transcriptome data. These findings provide fundamental data and a theoretical basis for further elucidating the pathogenic mechanism of GAstV-2 and developing targeted prevention and control strategies against gosling gout.