The issue of keel bone deformities and abnormalities is different depending on various housing systems for the birds. Keel fractures have received a lot of attention lately because of the increase in “cage-free” production in the egg industry. European researchers have led a lot of studies on the issue of keel fractures in aviary systems, but North American scientists have also been studying the issue as well.
The research and observations will be related to the conventional cage system. Of course, nutritional solutions are also very important. The final portion of this contribution relates to providing data and commercial experience to address some common misperceptions in the industry.
The nutritional solutions are answers determined to benefit MFI in the feeding program. The information is more validations of previous studies and recommendations by consultants than novel ideas. The aim is to provide more specifics with clear results under more commercial-type conditions. The bird observations and myth-busting claims relative to nutritional studies and programs at MFI will be discussed at the end of this article.
The nutritional studies/experiences will be divided into three parts: 1) Vitamin D (levels and sources), 2) Calcium (level and sources), and 3) aluminosilicates. The research is focused primarily on Bovans White birds. Although soft bones and keel deformations can be observed with any strain of bird, at MFI we have historically had more soft bone issues with Bovans birds. Hence, the strain of bird was used as a model to minimize strain as a variable in the studies.
The typical industry recommendation for vitamin D3 for laying hens is 3,000,000 IU/ton. However, Matilla et al. (2004) reported that tibia breaking strength is increased at 68 weeks of age when about double this amount of vitamin D3 was fed starting at 20 weeks of age. Preliminary studies at the Wakefield facility in commercial houses showed that keel tip softness in Bovans birds could be further decreased by adding additional vitamin D3 premix to the diet during peak production. The decision was made at MFI to increase the vitamin D3 content in the vitamin premix to provide 6,000,000 IU/ton of feed rather than 3,000,000 IU/ton. A vitamin D source trial was conducted at a “project house”, which houses approximately 500 birds in cages similar to the system used in some of the commercial houses.
The basal diet was a typical corn-soybean meal-meat and bone meal-DDGS diet used in the formulation program. The control group was fed 6,000,000 IU/ton vitamin D3 (all spray-dried). Treatment 2 consisted of adding 4,000,000 IU/ton more vitamin D3 in the spray-dried form. Treatment 3 consisted of adding 25-OH D3 (Hy-D from DSM) at the manufacturer’s recommendation of 69 ug/kg. This level of Hy-D would be equivalent to adding 2,500,000 IU/ton if compared directly to vitamin D3 activity. Edwards et al. (1994) reported that 800 ICU/kg (20 ug/kg) vitamin D3 yielded similar protection against rickets incidence and improved tibia bone ash the same as exposing broiler chicks to ultraviolet light.
Ledwaba and Roberson (2003) reported a similar result in these parameters when 10 ug/kg 25-OHD3 was fed to broiler chicks in place of exposure to ultraviolet light. Thus, the relative biological activity of 25-OH D3 to vitamin D3 is about 2x. Hence, the Hy-D addition to the diet in this trial would be equivalent to adding 5,000,000 IU/ton.
The birds were fed the treatments from housing in the project house at 16 weeks of age to 30 weeks of age. There were no differences in production parameters or keel bone softness between vitamin D sources, but keel tip softness was higher in the control group fed 6,000,000 IU/ton compared to birds fed additional vitamin D activity. Kim et al. (2011) reported that cortical bone mineral content of broiler femurs was increased when vitamin D3 was fed at 9,000,000 IU/ton. There was no mortality in the trial, demonstrating that keel bone softness is not related to mortality observed in early lay when soft bones are diagnosed in necropsy of mortality in commercial houses.
This directly busts the myth spread by some members of the egg industry that birds with soft birds will suddenly die from cage-layer fatigue in peak production. The Hy-D treatment was about 7x the cost of adding spray-dried vitamin D3 to the diet.
Dietary calcium level in peak production has typically been targeted to reach 4.3 g/day in peak production which is slightly above breeder guidelines of 4.1-4.2 g/day. The proportion of large particle limestone contributing to the dietary calcium provided is usually 40-45 % in peak production. Dietary available phosphorus is typically fed at about 500 mg/d in peak production, but may be fed at a 5-10% higher level for Bovans birds. An additional factor for MFI to consider is the recycling of dried eggshells from breaker plants to use as a calcium source in the diets. The solubility of eggshells may be lower than the used fine particle of limestone, which contributes another factor to consider when feeding to prevent soft keel tips and keel deformities.
The use of a minimum of 20 lb/ton fine limestone instead of relying completely on eggshells for small particle calcium has been a vital part of the formulation program to reduce soft bone issues in peak production. Eggshell solubility has been shown to improve if the shells are ground to a level of about 250 um. Cheng and Coon (1990a) reported that solubility of limestone affects bone structure in layers. Pulverized limestone with 47% solubility fed to layers resulted in high tibia bone ash in peak production. Solubility of eggshells may be about half this amount.
Research has shown that cortical bone ash weight will be increased at 4.5 g/day calcium consumption compared to 4.0 g/day or lower. Studies in the same laboratory showed that bone strength can be improved in laying hens if dietary calcium is fed at 5.0 g/day vs. 3.5 g/day. Recent changes in the MFI feeding program has resulted in lower soft bones issues if dietary calcium is increased to 4.5-4.6 g/day by 25 weeks of age when the flock has reached peak production. This method allows for dietary calcium to be able to supply the amount of calcium needed to produce the shell on the egg. Large particle calcium is continually increased with age as the birds reach 50 weeks of age and older.
Several commercial trials on the use of the anti-caking agent T-bind were run and improved bone structure as well as a positive effect on egg production were observed. The institution of a T-bind program minimized issues with mouth lesions that were prevalent when the author started working for MFI in 2005. Also a reduction in pasty vents was noticed. T-bind has been used to mitigate issues with mycotoxins in several areas of the country. The original trial was conducted using Hy-Line W36 birds. The percent of birds with soft keel tips was decreased when 6 lb/ton T-bind was fed, but more importantly the amount of severely soft tips was cut in half when either 3 or 6 lb/ton T-bind was fed in peak production. Ballard and Edwards (1988) reported that sodium aluminosilicate increased calcium absorption and 47Ca retention in broiler chicks. In a more recent trial with Bovans White birds, the addition of T-bind at two particles sizes (400 or 1100 um) as well as a similar level of Azomite (900 um) still reduced soft keel tip incidence even with changes regarding vitamin D3 and calcium level increases implemented to the program.
Observations and myth-busting
A general observation in several bone health studies has been the sudden increase in keel tip softness as the flock reaches peak production (25 weeks of age) indicating a negative calcium balance. Medullary bone is maintained at the expense of cortical bone during the period of calcium deficiency. The development of keel deformation would typically be seen as the birds reached about 35 weeks of age. Keel deformities can begin sooner if there is an environmental situation which results in reduced feed consumption as the birds are coming in peak production. The incidence of bone abnormalities can affect a large portion of the flock with no effect on egg production. This busts the myth that keel abnormalities will result in lower egg production. This belief refers to the claim by Nasr et al. (2013) that keel fractures will decrease egg production by 6%.
The incidence of keel abnormalities will also be reduced as the birds age even during peak production without affecting egg production. This busts another myth that birds must go out of production to heal soft bones. Mortality was almost non-existent during peak production and any dead bird found had very strong bones. There was absolutely no correlation between soft bones and mortality in peak production which busts another myth in the industry that birds found dead with some softness in the bones but no other issues diagnosed must have died from cage-layer fatigue. In a university research trial, conducted about 15 years ago, laying hens had to be fed a diet that was very deficient in phosphorus for several months before mortality was observed due to nutrient deficiency. An important observation in current studies was that soft keel tips that are not severe will completely heal. Severely soft tips will result in bent tips and curvature at the end of the keel tip and possibly a broken keel tip. Keel curvature starts with a deviation in the keel bone which can occur at different areas of the keel, but usually in the mid-section of the bone. Mild deviations will typically heal while severe deviations eventually begin to bend into the S-shaped curve identified with keel curvature. These changes can occur over a one-week period and is very sensitive to changes in feed intake. A change of 5-8% in feed intake has a large influence on changes in keel abnormalities. These changes may not even be noticed if the birds on fed on a phase-feeding program where changes are made monthly or longer.
The observation that birds can heal and continue to grow bone in peak production busts the myth that once birds have keel deformations the birds can never fully recover and replace lost trabecular bone tissue and agrees with Zhang (1994) that bone growth can continue to occur in peak production. Osteoclastic activity predominates during active shell formation and osteoblastic activity is more dominant when the shell gland is inactive. Keel abnormalities continue to be a concern for poultry companies as we consider it to be a welfare issue for the bird (although they exhibit no pain during keel palpation). The long-term effects of soft and bent keels on bird health during post-peak are being evaluated more directly in current studies. The primary take-home message is that high levels of keel abnormalities can be observed during peak production with no effect on egg production or mortality and non-severe keel abnormalities can be quickly healed in laying hens with no pause in egg production.
References are available on request
From the Proceedings of the Midwest Poultry Federation Convention