Subclinical necrotic enteritis (NE) is primarily caused by the gram-positive bacterium, Clostridium perfringens (Cp). The trend towards removal of in-feed antimicrobials and subsequent increased emergence of infection in poultry has resulted in a wide interest in better understanding of the mechanism behind this disease. The virulence of NE, to a large extent, depends on the virulence of Cp strains. Thus, this study was to assess how 2 different strains of Cp affect performance and gut characteristics of broiler chickens. Ross 308 male broilers (n = 468) were assigned to a 2 × 3 factorial arrangement of treatments with antibiotics (Salinomycin at 72 ppm and zinc bacitracin at 50 ppm -, or +) and challenge (non-challenge, Cp EHE-NE18, or Cp WER-NE36). Oral administration of Eimeria oocysts (day 9) followed by inoculation with 1 mL 108 CFU Cp strains (day 14 and 15) were used to induce NE. Broiler performance was analyzed at day 10, 24, and 35. On day 16, intestinal lesion score and intestinal pH were evaluated and samples of cecal content were analyzed for bacterial counts and short-chain fatty acid concentrations (SCFA). Birds in both challenged groups showed higher feed conversion ratio (FCR), lower weight gain (P < 0.001), increased lesion scores in the jejunum (P < 0.01), and reduced pH in the ileum and cecum (P < 0.01), compared to the non-challenged birds. They also showed decreased numbers of Bacillus spp. (P < 0.001), and Ruminococcus spp. (P < 0.01) in the cecal content. On day 35, the NE36 challenged birds had a lower weight gain (P < 0.001) and higher FCR (P < 0.001) compared to the NE18 challenged birds. Interestingly, cecal Lactobacillus and lactate were increased by the NE challenge (P < 0.001), and to a greater extent in birds challenged with NE36 compared to the NE18 strain (P < 0.001). This study suggests that Cp strains varying in virulence produce different levels of disease in broiler chickens through modulating the gut environment, intestinal microbiota, and SCFA profile to different extents.

中文翻译：

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两种不同的产气荚膜梭菌菌株在肉鸡中产生不同程度的坏死性肠炎。

亚临床坏死性肠炎 (NE) 主要由革兰氏阳性菌产气荚膜梭菌 (Cp) 引起。去除饲料中的抗微生物剂和随后增加家禽感染的趋势导致人们对更好地了解这种疾病背后的机制产生了广泛的兴趣。NE的毒力在很大程度上取决于Cp菌株的毒力。因此，本研究旨在评估 2 种不同的 Cp 菌株如何影响肉鸡的生产性能和肠道特性。罗斯 308 只雄性肉鸡（n = 468）被分配到使用抗生素（72 ppm 盐霉素和 50 ppm - 或 + 锌杆菌肽）和攻击（非攻击，Cp EHE-NE18，或 Cp WER-NE36)。口服艾美球虫卵囊（第 9 天），然后接种 1 mL 108 CFU Cp 菌株（第 14 天和第 15 天）用于诱导 NE。在第 10、24 和 35 天分析肉鸡的性能。在第 16 天，评估肠道损伤评分和肠道 pH 值，并分析盲肠内容物样本的细菌计数和短链脂肪酸浓度 (SCFA)。两个攻击组的鸡只表现出较高的饲料转化率 (FCR)、较低的增重 (P < 0.001)、空肠损伤评分增加 (P < 0.01) 以及回肠和盲肠的 pH 值降低 (P < 0.01)。对未受挑战的鸟类。他们还显示芽孢杆菌属的数量减少。（P < 0.001）和瘤胃球菌属。(P < 0.01) 在盲肠内容。在第 35 天，受 NE36 攻击的鸡只增重较低（P < 0.001），FCR 较高（P < 0. 001) 与 NE18 挑战赛鸽相比。有趣的是，NE 攻击导致盲肠乳酸杆菌和乳酸增加（P < 0.001），与 NE18 菌株相比，NE36 攻击的鸡只增加了更大程度（P < 0.001）。本研究表明，毒力不同的 Cp 菌株通过不同程度地调节肠道环境、肠道微生物群和 SCFA 谱，在肉鸡中产生不同程度的疾病。