A Review on Pathophysiology, and Molecular Mechanisms of Bacterial Chondronecrosis and Osteomyelitis in Commercial Broilers

Abstract

Modern day broilers have a great genetic potential to gain heavy bodyweights with a huge metabolic demand prior to their fully mature ages. Moreover, this made the broilers prone to opportunistic pathogens which may enter the locomotory organs under stress causing bacterial chondronecrosis and osteomyelitis (BCO). Such pathogenic colonization is further accelerated by microfractures and clefts that are formed in the bones due to rapid growth rate of the broilers along with ischemia of blood vessels. Furthermore, there are several pathways which alter bone homeostasis like acute phase response, and intrinsic and extrinsic cell death pathways. In contrast, all the affected birds may not exhibit clinical lameness even with the presence of lameness associated factors causing infection. Although Staphylococcus, E. coli, and Enterococcus are considered as common bacterial pathogens involved in BCO, but there exist several other non-culturable bacteria. Any deviation from maintaining a homeostatic environment in the gut might lead to bacterial translocation through blood followed by proliferation of pathogenic bacteria in respective organs including bones. It is important to alleviate dysbiosis of the blood which is analogous to dysbiosis in the gut. This can be achieved by supplementing pro, pre, and synbiotics which helps in providing a eubiotic environment abating the bacterial translocation that was studied to the incidence of BCO. This review focused on potential and novel biomarkers, pathophysiological mechanism, the economic significance of BCO, immune mechanisms, and miscellaneous factors causing BCO. In addition, the role of gut microbiomes along with their diversity and cell culture models from compact bones of chicken in better understanding of BCO were explored.

Keywords: bacterial chondronecrosis and osteomyelitis (BCO); biomarkers; broiler; lameness; mesenchymal cells.

Figure 1

(A) Response of lipopolysaccharides (LPS) with respect to TNFα (tumor necrosis factor), and osteoclastic activity (B) TNFα, and osteoclastic activity in the presence LPS under the influence of TLR4 blockers (C) TNFα, and osteoclastic activity in the presence of RANKL under the influence of TLR4 blockers.

Figure 2

Known pathways through which bacterial chondronecrosis and osteomyelitis (BCO) is observed in modern day broilers.

Figure 3

Mechanisms during pre and postnatal development of chicken increasing incidence of BCO.

Figure 4

DICER 1 dysregulation in the presence of bacteria causing break in bone homeostasis.

Figure 5

Factors affecting incidence of lameness.