Bacterial chondronecrosis with osteomyelitis (BCO) was first reported in 1972 and is now recognized as an important factor to cause lameness in poultry production. Recent research in Northern Ireland indicated that 17.3% of birds with lameness has BCO lesions. Other research in the US showed that leg problems cost the commercial broiler industry between US$80 and $120 million annually.
During the last decade the lameness condition caused by bacterial infection has been reported with various names; femoral head necrosis, tibial head necrosis, proximal femoral degeneration, long bone necrosis but nowadays BCO is widely accepted as the common term for this condition.
BCO is a common cause of lameness in US and Europe that typically affects 1.5% of broilers grown starting at around 30 days of age. In Asia, the incidence of BCO may be lower at around 1%, as production cycles tend to be shorter, though subclinical issues and mortality do occur. Furthermore, BCO can contribute to product quality issues, e.g. consumers reject product where the white cap of articular cartilage separates from the femur head.
About 10-15% of broilers suffer from subclinical BCO, a condition that appears first in younger birds (Thorp et al., 1993). BCO increases mortality due to culling and selection, and results in lower body weight gain and higher FCR as affected birds suffer impaired mobility and are unable to move towards feeders and drinkers as frequently as they should.
BCO may be present and negatively influence flock performance and health even though it is not recognized as such. In one example, Prof Wideman cited a country he visited where multiple individuals claimed that BCO was not a problem locally. However, it turned out that 40% of the mortality in broilers domestically were being culled due to lameness caused by bacterial chondronecrosis with osteomyelitis. That means producers should be diligent: “In my opinion, wherever broilers are being grown, this [BCO] is going to be a problem—an important problem,” stated Prof Wideman.
BCO lameness is caused by bacterial infection of the femoral or tibial head, which can result in femoral and tibial head necrosis. Several research results showed that Staphylococcus spp., Enterococcus spp., E. coli and Mycobacterium spp. are the most common bacteria isolated from joint lesion in the birds with BCO lameness. As all of these bacteria above are members of the intestinal microbiota, these findings suggest the translocation of bacteria from the gut to the joints through the gut barrier.
From what we know of the pathogenesis of BCO, pathogenic bacteria (e.g. Staphylococcus spp., Enterococcus spp. and even E. coli) harbored in the gut gradually leak through the intestinal epithelium, make their way into the circulation and trigger the infections. Hence, the primary focus is to improve intestinal health and barrier function to protect against bacterial translocation responsible for BCO.
Intestinal bacteria in the lumen of the intestinal tract can penetrate into the lamina propria through the weakened physical barrier, and penetrated bacteria can move to the other organs including joint via the blood stream. Once the bacteria reach to the growth plates of long bones, they are harbored in microfractures and begin to destroy the bone minerals.
Tight-junction is the structure in the intestinal tract to seal the apical boundaries of enterocyte, which consist of more than 40 proteins. Actin attachment in tight-junction enable it to close and open accordingly. It is one of the physical barriers in the innate immune system located in the intestinal tract, which prevents luminal antigens or bacteria from entering into mucosa and reaching into blood stream, resulting in bacterial translocation.
Disrupted tight junction as intestinal barrier is compromised in a variety of clinical symptoms, such as lameness from chondronecrosis and spinal cord related neurological sign from osetomyelitis. Although the working mechanism of tight-junction is not clearly determined, it is obvious that the regulation of the tight-junction is closely regulated by the beneficial microbiota in the gut. The colonization of the gut with poultry probiotics can help reduce the translocation of pathogens into the bloodstream. Some studies suggested the possibility to regulate the tight-junction with methionine and cinnamaldehyde, but these nutritional approaches are still controversial.
Regulation of tight-junction can be impaired by several factors, including dysbiosis, mycotoxin and stress. Dysbiosis is defined as a disturbed intestinal microbiota composition, which has emerged as the most common intestinal problem in poultry production. As intestinal microbiota play a critical role in maintaining intestinal homeostasis, including tight-junction, dysbiosis condition impaired the tight-junction regulation resulting in leaky gut. Several mycotoxin including Deoxynivalenol (DON), Fumonisin (FUM) and Aflatoxin B1 (AFB1) can also impair the gene expression for protein to consist of tight-junction, resulting in increased permeability of intestinal epithelium. Recent research indicated that high level of glucocorticoid from chronic stress can down regulate the expression of tight-junction related protein (claudin-1).
Figure 1. Villi in intestinal tract and tight-junction structure (Arrow), Picture from Bohórquez et al, 2011
Probiotics can help to minimize the BCO lameness by reduction of bacterial translocation from the gut. In in-vivo trial conducted in Arkansas with wire-flooring model, Prof. Robert Wideman showed that broilers reared on wire flooring consistently had higher incidences of lameness than hatch-mates reared on wood-shavings litter and adding probiotics to the diet beginning at 1 day of age consistently reduced the incidence of lameness for broilers reared on wire flooring.
These experiments indicate that probiotics administered prophylactically may constitute an alternative to antibiotics for reducing lameness attributable to BCO. The immunomodulation effect of the beneficial microflora with probiotic also helps the birds counteract this problem more efficiently.
“A healthy gut is the backbone of performance,” according to Luis Valenzuela, Product Manager at BIOMIN.
Extensive research has identified 3 types beneficial bacteria that acts as drivers of good gut health in poultry, each inhabiting various parts of the gastrointestinal tract:
They act to competitively exclude harmful bacteria in the gut, prime the immune system and create a proper environment for beneficial microflora.
All three strains are found in PoultryStar® – a well-defined, poultry-specific, multi-species synbiotic product developed by BIOMIN that is the only one of its kind with EU authorization. Mycotoxin deactivators or toxin binders in poultry feed can also reduce the bacterial translocation from tight-junction loosening caused by several mycotoxins.
PoultryStar® is a well-defined, multi-species poultry probiotic plus prebiotic (synbiotic) that promotes a beneficial gut microflora and improves the results of broilers, layers and breeders.
Bacterial chondronecrosis with osteomyelitis and lameness in broilers: a review. Poult Sci. 95 (2)
Molecular Survey of Bacterial Communities Associated with Bacterial Chondronecrosis with Osteomyelitis (BCO) in Broilers. PLoS ONE 10 (4)
Bacterial chondronecrosis with osteomyelitis ('femoral head necrosis') of broiler chickens. Avian Pathology 29
Cinnamicaldehyde regulates the expression of tight junction proteins and amino acid transporters in intestinal porcine epithelial cells. Journal of Animal Science and Biotechnology 8:66
A wire-flooring model for inducing lameness in broilers: Evaluation of probiotics as a prophylactic treatment. Poultry Science 91 (4)
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