Department of Animal and Food Sciences, Oklahoma State University, Stillwater, Oklahoma, USA.
Microbiol Spectr. 2024 Oct 3;12(10):e0082324. doi: 10.1128/spectrum.00823-24. Epub 2024 Sep 9.
is a major cause of coccidiosis in chickens and a key predisposing factor for other economically significant diseases such as necrotic enteritis. However, a detailed understanding of the intestinal microbiome response to infection is still lacking. This study aimed to comprehensively investigate the dynamic changes of the intestinal microbiome for 14 days post-infection (dpi) with . Bacterial 16S rRNA gene sequencing was performed with the ileal and cecal digesta collected from mock and infected chickens at the prepatent (3 dpi), acute (5 and 7 dpi), and recovery phases (10 and 14 dpi) of infection. Although no notable changes were observed at 3 dpi, significant alterations of the microbiota occurred in both the ileum and cecum at 5 and 7 dpi. By 14 dpi, the intestinal microbiota tended to return to a healthy state. Notably, was enriched in response to infection in both the ileum and cecum, although individual , , and species varied in the temporal pattern of response. Concurrently, major short-chain fatty acid-producing bacteria, such as , were progressively suppressed by in the cecum. On the other hand, opportunistic pathogens such as , , and were significantly enriched in the ileum during acute infection.
We have observed for the first time the dynamic response of the intestinal microbiota to infection, synchronized with its life cycle. Minimal changes occur in both the ileal and cecal microbiota during early infection, while significant alterations coincide with acute infection and disruption of the intestinal mucosal lining. As animals recover from coccidiosis, the intestinal microbiota largely returns to normal. -induced intestinal inflammation likely creates an environment conducive to the growth of aerotolerant anaerobes such as , as well as facultative anaerobes such as , , and , while suppressing the growth of obligate anaerobes such as short-chain fatty acid-producing bacteria. These findings expand our understanding of the temporal dynamics of the microbiota structure during infection and offer insights into the pathogenesis of coccidiosis, supporting the rationale for microbiome-based strategies in the control and prevention of this condition.
是鸡球虫病的主要原因，也是坏死性肠炎等其他经济上重要疾病的关键诱发因素。然而，人们对感染后肠道微生物组的反应仍缺乏详细的了解。本研究旨在全面调查感染后 14 天内（dpi）鸡的肠道微生物组的动态变化。用盲肠和回肠内容物进行细菌 16S rRNA 基因测序，盲肠和回肠内容物分别来自感染前（3dpi）、急性（5dpi 和 7dpi）和恢复期（10dpi 和 14dpi）的模拟和感染鸡。尽管在 3dpi 时没有观察到明显的变化，但在 5dpi 和 7dpi 时，盲肠和回肠中的微生物群都发生了显著的变化。到 14dpi 时，肠道微生物群趋于恢复健康状态。值得注意的是，在回肠和盲肠中，都有 被富集以响应 感染，尽管个体 、 和 物种的反应模式在时间上有所不同。同时，主要的短链脂肪酸产生菌，如 ，在盲肠中被 逐渐抑制。另一方面，机会性病原体，如 、 和 ，在急性感染期间在回肠中显著富集。
我们首次观察到肠道微生物群对 感染的动态反应，与它的生命周期同步。在早期感染过程中，回肠和盲肠微生物群几乎没有变化，而在急性感染和肠道黏膜破坏时，会发生明显的变化。当动物从球虫病中恢复时，肠道微生物群在很大程度上恢复正常。 引起的肠道炎症可能为需氧兼性厌氧菌，如 ，以及兼性厌氧菌，如 、 和 等的生长创造了有利的环境，同时抑制了短链脂肪酸产生菌等专性厌氧菌的生长。这些发现扩展了我们对 感染期间微生物群结构的时间动态的理解，并为球虫病的发病机制提供了新的见解，支持了基于微生物群的策略在控制和预防这种疾病方面的合理性。
