van der Sluis Malou, van Zeeland Yvonne R A, de Greef Karel H
Wageningen Livestock Research, Wageningen University & Research, Wageningen, Netherlands.
Division of Zoological Medicine, Department of Clinical Sciences, Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands.
Front Vet Sci. 2024 Feb 7;11:1354651. doi: 10.3389/fvets.2024.1354651. eCollection 2024.
Digestive problems, both those with a clear pathogenic origin (e.g., ) and those without obvious pathogen involvement [e.g., syndromes like epizootic rabbit enteropathy (ERE)], are common in production rabbits and account for the majority of losses in meat rabbit production. A multitude of nutritional, genetic and housing factors have been found to play a role in the occurrence of digestive problems. However, the exact early pathophysiological mechanism, including the links between aforementioned risk factors and subsequent development and expression of gastrointestinal disease, is less clear, especially in non-specific enteropathies without obvious pathogen involvement. In this review, we aim to shed more light on the derailment of the normal gastrointestinal functioning in rabbits. We discuss a conceptual integrated view of this derailment, based on an "overload" pathway and a "chymus jam" pathway, which may occur simultaneously and interact. The "overload" pathway centers around exposure to excess amounts of easily fermentable substrate (e.g., starch and protein) that might be incompletely digested prior to entering the caecum. Once there, hyperfermentation may result in changes in caecal pH and inhibition of the normal microflora. The second pathway centers around a chymus jam resulting from a compromised passage rate. Here, reduced hindgut motility (e.g., resulting from stress or limited fiber supply) leads to reduced flow of digesta and increased caecal retention times, which might lead to the production of abnormal caecal fermentation products and subsequent inhibition of the normal microflora. A central role in the presumed mechanism is attributed to the . We discuss the suggested mechanisms behind both pathways, as well as the empirical substantiation and alignment between theoretical concepts and observations in practice. The proposed hypotheses may explain the effect of time-based restriction to prevent ERE, which is widely applied in practice but to date not really understood, and suggest that the particle size of fiber may be a key point in the normal functioning of the colon and . Further insight into the circumstances leading to the derailment of physiological processes in the rabbit hindgut could provide a meaningful starting point to help improve their gastrointestinal resilience.
消化问题在商品兔中很常见,无论是有明确致病源的(如 )还是无明显病原体参与的(如兔流行性肠病综合征),这些问题在肉兔生产中造成了大部分损失。人们发现许多营养、遗传和饲养因素在消化问题的发生中起作用。然而,确切的早期病理生理机制,包括上述风险因素与随后胃肠道疾病的发展和表现之间的联系,尚不清楚,尤其是在无明显病原体参与的非特异性肠病中。在本综述中,我们旨在更深入地了解兔子正常胃肠功能的紊乱。我们基于可能同时发生并相互作用的“过载”途径和“食糜堵塞”途径,讨论这种紊乱的概念性综合观点。“过载”途径围绕着暴露于过量易于发酵的底物(如淀粉和蛋白质)展开,这些底物在进入盲肠之前可能未被完全消化。一旦到达盲肠,过度发酵可能导致盲肠pH值变化并抑制正常微生物群。第二条途径围绕着因通过速率受损导致的食糜堵塞。在这里,后肠蠕动减少(如由应激或纤维供应有限导致)导致食糜流动减少和盲肠停留时间增加,这可能导致异常盲肠发酵产物的产生并随后抑制正常微生物群。假定机制中的核心作用归因于 。我们讨论了这两条途径背后的假定机制,以及理论概念与实践观察之间的实证依据和一致性。提出的假设可以解释基于时间的限制预防兔流行性肠病的效果,这在实践中广泛应用但迄今为止尚未真正理解,并表明纤维的颗粒大小可能是结肠正常功能和 的关键点。对导致兔后肠生理过程紊乱的情况的进一步了解可以为帮助提高其胃肠道恢复力提供有意义的起点。