Prebiotic galactooligosaccharide improves piglet growth performance and intestinal health associated with alterations of the hindgut microbiota during the peri-weaning period.

BACKGROUND: Weaning stress reduces growth performance and health of young pigs due in part to an abrupt change in diets from highly digestible milk to fibrous plant-based feedstuffs. This study investigated whether dietary galactooligosaccharide (GOS), supplemented both pre- and post-weaning, could improve growth performance and intestinal health via alterations in the hindgut microbial community. METHODS: Using a 3 × 2 factorial design, during farrowing 288 piglets from 24 litters received either no creep feed (FC), creep without GOS (FG-) or creep with 5% GOS (FG+) followed by a phase 1 nursery diet without (NG-) or with 3.8% GOS (NG+). Pigs were sampled pre- (D22) and post-weaning (D31) to assess intestinal measures. RESULTS: Creep fed pigs grew 19% faster than controls (P < 0.01) prior to weaning, and by the end of the nursery phase (D58), pigs fed GOS pre-farrowing (FG+) were 1.85 kg heavier than controls (P < 0.05). Furthermore, pigs fed GOS in phase 1 of the nursery grew 34% faster (P < 0.04), with greater feed intake and efficiency. Cecal microbial communities clustered distinctly in pre- vs. post-weaned pigs, based on principal coordinate analysis (P < 0.01). No effects of GOS were detected pre-weaning, but gruel creep feeding increased Chao1 α-diversity and altered several genera in the cecal microbiota (P < 0.05). Post-weaning, GOS supplementation increased some genera such as Fusicatenibacter and Collinsella, whereas others decreased such as Campylobacter and Frisingicoccus (P < 0.05). Changes were accompanied by higher molar proportions of butyrate in the cecum of GOS-fed pigs (P < 0.05). CONCLUSIONS: Gruel creep feeding effectively improves suckling pig growth regardless of GOS treatment. When supplemented post-weaning, prebiotic GOS improves piglet growth performance associated with changes in hindgut microbial composition.

Amelioration of salmonellosis in pre-weaned dairy calves fed Saccharomyces cerevisiae fermentation products in feed and milk replacer.

Salmonellosis is an insidious and potentially epidemic problem in pre-weaned dairy calves. Managing this disease, or any other diarrheal disease, is a financial burden to producers. Calf mortalities and medicinal treatments are overt costs of salmonellosis, while hidden costs include hampered weight gains and persistent intestinal colonization of the pathogen. In this study, we examined the anti-Salmonella effects of Saccharomyces cerevisiae fermentation products (SCFP) incorporated into both the milk replacer and the starter grain. In a blinded study, 2-8 day-old calves were fed SCFP (n=20 calves) or an SCFP-free Control (n=20 calves) for two weeks before and three weeks after experimental challenge with Salmonella enterica serotype Typhimurium. Following the challenge, calves were monitored for clinical signs and parameters associated with salmonellosis. Calves were then euthanized and examined for rumen development and intestinal Salmonella colonization. When compared to calves that received milk replacer and feed lacking SCFP, calves fed SCFP had fewer bouts of diarrhea and fever. Rumens from these calves were more developed, as measured by the length of papillae, which is consistent with the enhanced weight gain observed in this treatment group. Additionally, Salmonella intestinal colonization was reduced in SCFP-fed calves and Salmonella fecal shedding disappeared at an earlier stage in these calves. This study revealed that the combination of two proprietary S. cerevisiae fermentation products provide marked benefit for preventing the negative effects of salmonellosis in pre-weaned dairy calves, while also boosting productivity. The mechanism of action needs to be clarified, but it may be related to the observed decrease in colonization by the pathogen and increase in rumen development.

Venous cystic adventitial disease presenting as an enlarging groin mass.

Venous cystic adventitial disease is an exceedingly rare vascular disorder, with 12 cases reported in the past decade. A 60-year-old woman presented with a painful, palpable groin mass without leg swelling. She was initially thought to have a nonreducible inguinal hernia. A computed tomography scan was obtained that revealed a cystic mass involving the right common femoral vein. Previous imaging revealed that the mass had enlarged over time. In the operating room, the cyst wall was excised without compromising vein integrity. The patient had an uneventful recovery and her pain resolved. We review the presentation, diagnosis, and treatment of this condition. We believe that the rapid evolution of this lesion suggests that an unknown inciting factor triggers its onset and growth.

Tyk2 negatively regulates adaptive Th1 immunity by mediating IL-10 signaling and promoting IFN-gamma-dependent IL-10 reactivation.

The Jak, Tyk2, is activated in response to IL-12 and IFN-alphabeta and promotes IFN-gamma production by Th1-type CD4 cells. Mice deficient in Tyk2 function have been previously shown to be resistant to autoimmune arthritis and septic shock but are acutely susceptible to opportunistic pathogens such as Toxoplasma gondii. In this study, we show that Tyk2, in addition to mediating the biological effects of IL-12 and IFN-alphabeta, is an important regulator for the signaling and expression of the immunosuppressive cytokine IL-10. In the absence of Tyk2, Ag-reactive CD4 cells exhibit impaired IL-10 synthesis following rechallenge of T. gondii vaccine-primed mice. The impaired IL-10 reactivation leads to unopposed antimicrobial effector mechanisms which results in a paradoxically superior protection of immune Tyk2(-/-) mice against virulent T. gondii challenge. We further demonstrate that Tyk2 indirectly controls CD4 IL-10 reactivation by signaling for maximal IFN-gamma secretion. The unexpected role of IFN-gamma in mediating IL-10 reactivation by Th1 cells provides compelling evidence that conditions driving Th1 responses establish a negative feedback loop, which will ultimately lead to its autoregulation. Thus, Tyk2 can be viewed as a dual-function Jak, mediating both pro and anti-inflammatory cytokine responses.