Animal Bioscience and Biotechnology Laboratory, Agricultural Research Service (ARS), United States Department of Agriculture (USDA), Beltsville, MD 20705.
College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.
Avian Dis. 2020 Sep 1;64(3):386-392. doi: 10.1637/aviandiseases-D-19-00098.
Clostridium perfringens (CP) is the etiologic agent of necrotic enteritis (NE) in broiler chickens that is responsible for massive economic losses in the poultry industry in response to voluntary reduction and withdrawal of antibiotic growth promoters. Large variations exist in the CP isolates in inducing intestinal NE lesions. However, limited information is available on CP isolate genetics in inducing NE with other predisposing factors. This study investigated the ability of five CP isolates from different sources to influence NE pathogenesis by using an Eimeria maxima (EM) coinfection NE model: Str.13 (from soil), LLY_N11 (healthy chicken intestine), SM101 (food poisoning), Del1 (netB+tpeL-) and LLY_Tpel17 (netB+tpeL+) for NE-afflicted chickens. The 2-wk-old broiler chickens were preinfected with EM (5 × 103 oocysts) followed by CP infection (around 1 × 109 colony-forming units per chicken). The group of the LLY_Tpel17 isolate with EM coinfection had 25% mortality. No mortality was observed in the groups infected with EM alone, all CP alone, or dual infections of EM/other CP isolates. In this model of EM/CP coinfections, the relative percentages of body weight gain showed statistically significant decreases in all EM/CP groups except the EM/SM101 group when compared with the sham control group. Evident gut lesions were only observed in the three groups of EM/LLY_N11, EM/Del1, and EM/LLY_Tpel17, all of which possessed an essential NE pathogenesis locus in their genomes. Our studies indicate that LLY_Tpel17 is highly pathogenic to induce severe gut lesions and would be a good CP challenge strain for studies investigating pathogenesis and evaluating the protection efficacy for antibiotic alternative approaches.
产气荚膜梭菌（CP）是导致肉鸡坏死性肠炎（NE）的病原体，由于自愿减少和撤回抗生素生长促进剂，它给家禽业造成了巨大的经济损失。在诱导肠道 NE 病变方面，CP 分离株存在很大的差异。然而，关于 CP 分离株在诱导 NE 与其他诱发因素方面的遗传学信息有限。本研究使用柔嫩艾美耳球虫（EM）混合感染 NE 模型，研究了来自不同来源的五个 CP 分离株对 NE 发病机制的影响能力：Str.13（来自土壤）、LLY_N11（健康鸡肠道）、SM101（食物中毒）、Del1（netB+tpeL-）和 LLY_Tpel17（netB+tpeL+），用于感染 NE 的鸡。2 周龄肉鸡用 EM（5×103 个卵囊）预感染，然后用 CP 感染（每只鸡约 1×109 个菌落形成单位）。与 EM 混合感染的 LLY_Tpel17 分离株组有 25%的死亡率。单独感染 EM、单独感染 CP 或 EM/其他 CP 分离株双重感染的组均未观察到死亡。在 EM/CP 混合感染的模型中，除 EM/SM101 组外，所有 EM/CP 组的体重增长率相对百分比与假对照组相比均呈统计学显著下降。只有在 EM/LLY_N11、EM/Del1 和 EM/LLY_Tpel17 三组中观察到明显的肠道病变，这三组分离株的基因组中均存在必需的 NE 发病机制基因座。我们的研究表明，LLY_Tpel17 对诱导严重的肠道病变具有高度致病性，可作为 CP 挑战株，用于研究发病机制和评估抗生素替代方法的保护效果。
