It was estimated that the incidence of birds with leg problems was 2-6% (Figure 1). However, a late study found that, for example in the UK, more than 27% of birds on average had poor walking ability and as many as 3.3% of the birds were considered to be clinically lame (Dudley-Cash, 2014). It is time to have a closer look into the matter.
Usually lameness problems are blamed on the rapid genetic development in poultry production; however, BCO, formerly known as femoral head necrosis due to the destruction of the proximal femoral head, is a much more significant cause of lameness. Usually the disease is recognized to occur when birds are around 35 days old. Nevertheless, signs of the disease have been seen in birds ranging from 14 to 70 days of age (McNamee and Smyth, 2000).
What is BCO?
The disease is caused by bacteria. Most commonly Staphylococcus aureus, but other bacterial species found in field outbreaks of BCO also include Enterococcus spp., Escherichia coli, Salmonella spp. and Mycobacterium avium (Reece, 1992; Thorp et al., 1993; McNamee, 1998; McNamee et al., 1998). BCO usually starts to develop in the proximal femur and proximal tibiotarsus commonly known as the tibia in which the wide, thick growth plates are susceptible to mechanical damage or osteochondrosis (Figure 2 and 3).
The extent of bacterial translocation plays an important role when it comes to the outbreak of BCO. Of high importance in this process are the tight junctions, as they represent an intestinal barrier, sealing the surfaces of the epithelial cells. 'Leaky' tight junctions make it easier for not only pathogenic bacteria but also the commensal microflora to cross the gastrointestinal epithelium and this way enter the arterial circulation. Once bacteria have crossed this barrier they can easily distribute and infect the bone (Wideman, 2015).
However, the integrity of the existing tight junctions and the production of new tight junction proteins can be influenced. Those influencing factors are physiological stress but also the direct cell-to-cell signaling in between the epithelial cells and commensal or pathogenic bacteria in the gastrointestinal tract (Saunders et al., 1994; Ando et al., 2000; Steinwender et al., 2001; Ulluwishewa et al., 2011; Pastorelli et al., 2013). Factors such as heat stress or microbial challenges can influence the integrity of the tight junctions significantly and may lead to an increased movement of pathogenic bacteria across the epithelial wall (Quinterio-Fiho et al., 2010, 2012a, 2012b; Murugesan et al., 2014). After bacterial proliferation, an immunological response follows which generates the necrotic abscess and voids that are pathognomonic for BCO (Wideman and Prisby, 2012; Wideman and Pevzner, 2012). In simple words, harmful bacteria getting through the gastrointestinal epithelium will affect the musculoskeletal system of birds resulting in lameness.
How can probiotics be a helpful tool in preventing lameness in poultry?
Several studies have shown that probiotics can alleviate dysfunctions in the intestinal barrier in poultry suffering from different stress factors such as heat, handling of the birds for the purpose of weighing or moving, vaccination, beak trimming, stocking density or bacterial challenge (Sohail et al., 2010, 2012; Murugesan et al., 2014; Song et al., 2014).
There are several ways probiotics alleviate BCO. Probiotics alter the microbial population within the gastrointestinal tract, reducing pathogenic bacteria and increasing the level of beneficial bacteria in turn. This is because probiotics improve gut health and integrity, but probiotics also have positive effects on the immune system, which means pathogenic bacteria which have already crossed the epithelial cell wall together with the common bacteria found in the microflora can be eliminated easier (Wideman, 2016).
Studies of probiotic activity in recent years also provide evidence that probiotics counter gastrointestinal inflammation by affecting the epithelial cell function, including epithelial cell barrier function, epithelial cytokine secretion, and their antibacterial effects relating to colonization of the epithelial layer. In addition, there is emerging evidence that probiotics induce regulatory T-cells that act as a break on the effector T-cells that would otherwise cause inflammation (Boirivant and Strober, 2007).
However, even so there are still a lot of open questions on how exactly probiotics influence the occurrence of BCO, it has to be mentioned that studies (Wideman et al., 2015) have shown that not all probiotics exert positive effects on the occurrence of BCO.
Effect of B-Act® on BCO
To see if B-Act® is one of the probiotics that can help decrease the incidence of BCO, a trial was conducted at the Poulpharm research facility in Belgium using 120 ross 308 broilers housed on wire flooring for 53 days to induce BCO as no bacterial challenge was applied. Birds were randomly assigned to the following three groups:
- a control group
- a group receiving an antibiotic from day 38 to day 47
- a group supplemented with B-Act® (a probiotic product from Huvepharma® which contains viable spores of a strain of Bacillus licheniformis, DSM 28710) at 0.5 lb/ton (1.6 x 106 cfu/g of feed) to the diet from start to finish.
The trial showed that the addition of the antibiotic or B-Act® to the diet of broilers affected the occurrence of lameness in BCO induced broilers significantly (p < 0.05; Figure 4). Even though the addition of the antibiotic resulted in a numerically slightly lower lameness percentage compared to the B-Act® group, the onset of lameness took place around the same time. The onset of lameness was defined as the day when 3% of the birds were visually lame. The first incidences of lameness were reported at day 40 in the control group, while in the B-Act® and the antibiotic treated group, the onset of lameness took place on day 45 and 46, respectively.
The supplementation of certain probiotics to the diet may help reduce BCO and the significance the disease has on the economical profit of poultry operations.