Early detection and interventions for lameness in broilers

The prevalence of leg weakness has been a growing concern in the poultry industry, it is estimated that 5.5 – 48.8% of birds have compromised gait (Hartcher and Lum, 2020). Lameness can result from a multitude of factors (Casaubon Huguenin and Brugère-Picoux, 2015, Shivaprasad, et al., 2013, McNamee and Smyth, 2000, Wideman, 2016) including:

1. developmental abnormalities,
2. toxicity,
3. viral infections,
4. dietary deficiencies, and
5. bacterial infections.

The focus of this article is on dietary and bacterial challenges that can predispose birds to lameness. It is important to note that lameness is a progressive disease so with monitoring it can be reduced in a flock.

Dietary lameness

Proper bone development is central for structural integrity and muscle deposition which ultimately indicates meat yield. Calcium (Ca), phosphorus (P), and vitamin D3 (vit D3) are key players in mineralization as part of bone development. Ca and P are the structure, strength, and flexibility of the bone while vitamin D supports the transport of these minerals from the gut to the bone.

Dietary sources of these components are relatively inexpensive, but accurately providing the components to the bird at their requirements can be challenging. For example, digestible Ca has been topic receiving much attention due to a general oversupply of total dietary Ca (Walk, 2016) and associated detrimental effects on P and amino acid utilization and performance (Walk et al., 2021). It has been well documented that dietary Ca can form mineral-phytate complexes, ultimately impacting phytate degradation and P availability (Selle et al., 2009). Additionally, vit D3 can be supplemented in different forms. The inactive form of Vit D (cholecalciferol) can be produced in the skin or absorbed from the diet. It undergoes 2 hydroxylation steps to become hormonally active: 1) firstly, in the liver to 25-hydroxycholecalciferol (25-OH-D3) and 2) secondly, in the kidneys and intestine to 1α,25-dihydroxycholecalciferol (1,25-OH-D3). Once in the active form, it can support the absorption of Ca and P in the gut (Sakkas et al., 2019). Intestinal and/ or liver damage (by mycotoxins or other challenges) causes the inability for vit D absorption, directly impacting the bioavailability of nutrients for proper bone formation (Keçi, et al., 2019). Dietary 25-OH-D3 is absorbed more efficiently than cholecalciferol (Figure 1) and is more effective to improve skeletal health as indicated by gait score (Figure 2; Sakkas et al., 2019).

Evaluating blood levels of Ca, P, and 25-OH-D3 can be indicators of skeletal health and having proper baseline data for these at each life stage it key. As an example, a broiler breeder producer was seeing increased mortality in young birds after feeding and suspected a P problem; however, after taking blood samples and comparing with the Verax™ reference database, the birds were experiencing low Ca. By incorporating oyster shells and 25-OH-D3, and improving ventilation, the producer avoided further losses.

Bacterial lameness

Wet litter can predispose birds to footpad dermatitis and hock burns which is associated with lameness (Granquist et al., 2019) and wet litter can be a result of dietary challenges. However, the most common lameness associated with bacteria is bacterial chondronecrosis with osteomyelitis (BCO). BCO lameness effects at least 1% of broiler production across the Americas, Europe, and Asia (Wideman, 2016). This lameness can lead to various production losses like lower body weight gain and increased condemnations (Granquist et al., 2019). For BCO to occur, bacteria travel from the gut through the bloodstream and reside in mechanical stress sites in the bone (Wideman et al., 2015). This type of lameness is exacerbated with a fast growth rate and poor intestinal integrity which allows for more bacterial leakage into the bloodstream.

Physiological stress and elevated serum corticosterone level can suppress the immune system allowing for more bacterial translocation across the intestine (Quinteiro-Filho et al., 2012). Poor intestinal integrity is also common with feed contaminated with mycotoxins. The 2023 dsm-firmenich world mycotoxin survey indicated that over 80% of poultry feed is contaminated with at least one mycotoxin, affecting the intestinal integrity of most commercial flocks.

Previously, providing a blanket antimicrobial or antibiotic growth promotors (AGPs) could mask the effects of poor intestinal integrity and function or a weak immune system. As AGPs have been reduced or removed from the poultry market for nontherapeutic purposes, there is an opportunity for a microbial imbalance (Adedokun and Olojede, 2019). Some bacterial strains are targeted as aggravators for BCO and may be present in parent stock, hatcheries, and throughout production. A few examples of bacteria that have been isolated from BCO lesions include Enterococcus spp. and Staphyloccocus spp (Gilley et al., 2014). Competitive exclusion throughout production using synbiotics (a combination of probiotics with prebiotics) has been shown to reduce the incidence of BCO (Figure 3; Wideman et al., 2012).

Dietary interventions for lameness

The importance of good nutrition with data-driven decision-making can make a difference in improving welfare and reducing economic downsides. Distinguishing the nutritional and bacterial causes of lameness can help fine tune which mitigation strategy is best for the flock.