Wideman Robert F
University of Arkansas, Division of Agriculture, Fayetteville, AR, USA 72701
Poult Sci. 2016 Feb;95(2):325-44. doi: 10.3382/ps/pev320. Epub 2015 Nov 2.
This review focuses on a specific cause of lameness known as bacterial chondronecrosis with osteomyelitis (BCO) in broilers. Rapid increases in body weight impose excessive torque and shear stress on structurally immature epiphyseal and physeal cartilage, primarily in the proximal femora, proximal tibiae, and flexible thoracic vertebrae. Excessive mechanical stress creates osteochondrotic clefts among the chondrocytes of susceptible growth plates. These wound sites are colonized by hematogenously distributed opportunistic bacteria, culminating in the gross abscesses and necrotic voids that are pathognomonic for terminal BCO. Lameness attributable to characteristic BCO lesions can be reproduced by rearing broilers on wire flooring to create persistent footing instability and physiological stress, without the need to inoculate the birds with pathogenic bacteria that presumably are present but quiescent within the bird's microbial communities or in the environment. Experiments using the wire-flooring model revealed innate differences in the susceptibility of broiler lines to BCO, and demonstrated that BCO incidences can be reduced by prophylactically providing probiotics in the feed, by prophylactically adding 25-hydroxy vitamin D3 to the drinking water, or by therapeutically adding the antibiotic enrofloxacin to the drinking water. Hatchery and chick quality issues clearly influence the susceptibility of broilers to BCO. When broilers remain in a sitting posture for prolonged periods, the major arteries supplying their legs may be compressed. These episodes of inadequate blood flow may prevent chondrocyte maturation and trigger focal necrosis, thereby making the epiphyseal and physeal cartilage highly susceptible to osteochondrosis and BCO. Much remains to be revealed regarding the pathogenesis of BCO. Further revelations will be facilitated by the availability of the now-validated wire-flooring models that consistently trigger high incidences of BCO in experimental flocks.
本综述聚焦于肉鸡中一种名为细菌性软骨坏死伴骨髓炎(BCO)的跛行特定病因。体重的快速增加会给结构上未成熟的骨骺和生长板软骨施加过大的扭矩和剪切力,主要集中在股骨近端、胫骨近端和活动的胸椎。过度的机械应力在易感生长板的软骨细胞之间形成骨软骨裂。这些创伤部位会被经血源分布的机会性细菌定植,最终形成肉眼可见的脓肿和坏死腔,这是晚期BCO的特征性表现。通过在金属网上饲养肉鸡以造成持续的站立不稳和生理应激,可重现由典型BCO病变引起的跛行,而无需给鸡接种可能存在于鸡的微生物群落或环境中但处于静止状态的病原菌。使用金属网饲养模型的实验揭示了肉鸡品系对BCO易感性的内在差异,并表明通过在饲料中预防性添加益生菌、在饮水中预防性添加25-羟基维生素D3或在饮水中治疗性添加抗生素恩诺沙星,可降低BCO的发病率。孵化场和雏鸡质量问题显然会影响肉鸡对BCO的易感性。当肉鸡长时间保持坐姿时,供应其腿部的主要动脉可能会受到压迫。这些血流不足的情况可能会阻止软骨细胞成熟并引发局灶性坏死,从而使骨骺和生长板软骨极易发生骨软骨病和BCO。关于BCO的发病机制仍有许多有待揭示。现已验证的金属网饲养模型在实验鸡群中始终引发高发病率的BCO,这将有助于进一步揭示相关机制。