Factors Causing Poor Pigmentation of Brown-Shelled Eggs 1
Gary D. Butcher and Richard D. Miles2
Introduction
The first documented report of shell pigment loss in brown-shelled eggs was in 1944 when Steggerda and Hollander, while removing dirt from eggshells produced from a small flock of Rhode Island Red hens, made the surprising discovery that some of the brown pigment also rubbed off. This effect was even more evident when the eggs were rubbed vigorously. Most of the eggs gave up their pigment fairly easily except those possessing a glossy surface.
It is well established that no single factor is responsible for the loss of shell pigment in brown-shelled eggs. Variation in pigmentation among brown-shelled eggs is more pronounced in broiler breeders than in commercial brown egg-type layers. In flocks of broiler breeders, it is common to have a variation in eggshell pigmentation, resulting in hues ranging from dark brown to almost bleached white. This contrast occurs because genetic selection for uniform brown-colored eggs in broiler breeder flocks is of little importance compared to eggshells of commercial brown egg-type birds. Most commercial producers and university personnel serving the poultry industry understand that the loss of shell pigment from brown-shelled eggs can be caused by numerous factors. Many individuals, however, still prematurely jump to conclusions and blame shell pigment loss and variability on only a single factor. The most common scapegoat is infectious bronchitis. Statements such as “I know my hens had bronchitis because their shells are pale” or “All you have to do to determine if your hens had bronchitis is to look at their eggshell color—if the shells are pale they had a bronchitis challenge” are still often heard in the field. Such statements are made even without knowledge of the flock’s bronchitis antibody titer, bronchitis vaccination schedule, or supporting necropsy findings.
More often than not, the cause of shell pigment loss is not bronchitis but some stressor to which the flock has been exposed. Fear, for example, is a common cause of eggshell pigment loss. It is not until all the contributing factors to pigment loss are considered that the exact reason can be identified and the problem resolved. Many times the exact cause of periodic, flock-wide pigment loss is never identified.
The purpose of this article is to identify and discuss the various factors that are known to contribute to the loss of eggshell pigment. A general review, however, of the pigments and the process involved in their deposition aids the reader in better understanding shell pigmentation problems.
Eggshell Formation and Pigment Disposition
Once the egg reaches the site of the reproductive tract known as the uterus (shell gland), it resides there for approximately 20 hours. During this time, the shell is deposited, mostly as calcium carbonate, onto the shell membranes that envelop the albumen and yolk. As shell formation progresses in the brown egg layer, the epithelial cells lining the surface of the shell gland begin to synthesize and accumulate the pigments. The three main pigments are biliverdin-IX, its zinc chelate, and protoporphyrin-IX. The most abundant pigment in today’s commercial brown-shelled eggs is protoporphyrin-IX. It is not until the final 3 to 4 hours of shell formation that the bulk of the accumulated pigment is transferred to the protein-rich, viscus fluid secretion known as the cuticle. The degree of brownness of the hen’s eggshell is dependent on the quantity of pigment directly associated with the cuticle. The pigment-rich cuticle is deposited onto the eggshell at about the same time shell deposition reaches a plateau, about 90 minutes prior to oviposition. Therefore, pigment distribution is not uniform throughout the thickness of the eggshell. Even though the eggshell contains traces of pigment, its contribution to the intensity of brown color is negligible compared to that of the cuticle.
Factors Responsible for Decreasing the Intensity of Brown Shell Color
Stress
Since the majority of the pigment is localized in the cuticle, anything that interferes with the ability of the epithelial cells in the shell gland to synthesize the cuticle will affect the intensity of eggshell pigmentation. This is especially true during the final 3 to 4 hours of shell deposition since it is during this time in the egg-laying cycle that cuticle synthesis and accumulation occur most rapidly.
Stressors in poultry flocks, such as high cage density, handling, loud noises, etc., will result in the release of stress hormones, especially epinephrine. This hormone, when released into the blood, is responsible for causing a delay in oviposition and the cessation of shell gland cuticle formation. The above stressors, which result in hen nervousness and fear, can cause pale eggshells to be produced. The paleness is often the result of amorphous calcium carbonate deposited on top of a preexisting fully formed cuticle or of an incomplete cuticle caused by premature arrest of cuticle formation.
Brown-shelled birds, especially broiler breeders, housed in experimental floor pens for research purposes often become fearful each time the pen is entered for such things as egg collection, vaccination, uniformity, and frame and fleshing measurements. When this occurs, production of pale-shelled eggs should be expected, especially if the fearfulness occurs during the last 3 to 4 hours of the egg-laying cycle when the cuticle formation is interrupted. In fact, the relationship between stress and the production of pale eggs by laying hens is so great that researchers have suggested that loss of shell pigment may provide a basis for a noninvasive method of assessing stress in hens.
Age of the Bird
As the brown egg-type bird ages, there is a corresponding decrease in eggshell pigment intensity. The exact reason for this is unknown. It is possibly due to the same quantity of pigment being dispersed over a larger surface area of shell as egg size increases with bird age or less pigment synthesis. As the hen ages it is normal for the tapered end of the egg to contain less pigment than the rounded end. Stress-related egg retention in the shell gland and subsequent amorphous calcium carbonate deposition on the shell surface have been identified as a major cause of pale eggs in older hens.
Chemotherapeutic Agents
A rapid decline in shell pigmentation is common following the ingestion of certain drugs by the hen, such as the sulfonamides. The coccidiostat Nicarbazin, administered to hens at a dose of 5 mg per day, can result in the production of pale eggs within 24 hours. Higher doses can lead to complete depigmentation of the eggshell cuticle.
Disease
Viral diseases, such as Newcastle and infectious bronchitis, affect egg production in poultry. These viruses have a specific affinity for the mucus membranes of the respiratory and reproductive tracts. Because the virus directly infects and damages the reproductive tract, the signs of disease are manifested indirectly in the product of the tract, the egg. Thus, total egg numbers decline and eggshells become thinner and abnormally pale and have irregular contour. Internal quality is also adversely affected (watery whites). These egg production and quality problems can persist for extended periods.
Summary
Most eggshell pigments are located in the cuticle and outer portion of the calcified eggshell. Premature arrest of cuticle formation or release of stress-related hormones (epinephrine) will result in the production of pale brown-shelled eggs. Age of the bird, use of certain chemotherapeutic agents, and disease also can affect the intensity of pigmentation. No one factor, especially infectious bronchitis, should be diagnosed as the cause of the reduced pigmentation of eggshells until all possible differentials that may affect pigmentation have been considered.
References
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NAE producers need to focus on Eimeria oocysts for more effective control of coccidiosis, necrotic enteritis, ByDon Waldrip, DVM Senior Technical Service Veterinarian Zoetis
Poultry producers raising broilers for the “no antibiotics ever” (NAE) market continue to find themselves battling necrotic enteritis (NE). Too often, this raises the ethical dilemma of deciding whether to render antibiotic treatment to birds with NE if the company doesn’t have a fallback option for medicated birds.
This difficult situation underscores the need to focus on controlling Eimeria oocysts to prevent coccidiosis, which goes hand in hand with NE.
Program options
Coccidiosis vaccination has grown tremendously in recent years. If this is your coccidiosis-control method of choice, do whatever you can to ensure good results. For instance, increased light intensity at the hatchery after coccidiosis vaccination and prior to farm delivery should encourage preening and ingestion of vaccinal oocysts.
Some producers are finding it helpful to follow the initial vaccine with a field boost sprayed on litter or feed.
Another approach is to use coccidiosis vaccination during warmer weather, when there’s generally less coccidial pressure, and then switch to non-ionophore anticoccidials during colder months.
A third option for NAE-production schemes is the so-called bio-shuttle program, where either in ovo or vaccination at day of age is followed by a non-ionophore anticoccidial administered. Controlled studies show this hybrid approach can reduce the incidence of coccidiosis in NAE birds, which in turn leads to fewer NE lesions, less mortality and better feed conversion.1 Timing of the medication is vitally important so it’s a good idea to enlist input from your flock veterinarian, who can help devise the best plan of action. If the anticoccidial is administered too soon, it will kill the vaccine’s coccidial oocysts before they cycle and birds won’t develop the necessary immunity. On the other hand, if the medication is administered too late, Clostridium infection may develop, leading to NE.
NAE producers who don’t use coccidiosis vaccines must rely solely on non-ionophore anticoccidials. With so few options in the toolbox, it becomes even more important to closely monitor the situation with regular posting sessions.
Another useful tool is anticoccidial-sensitivity testing, or AST. Monitoring enables strategic production selection and rotation, which will help preserve the efficacy of anticoccidials. Access to AST has become a bit difficult and may be considered costly for smaller producers, but when possible, I highly recommend it be practiced strategically.
Bird size matters
NAE producers growing smaller birds may find they need to rotate non-ionophore anticoccidials more often for the simple reason that farms processing birds after 5 to 6 weeks have more frequent cycles of exposure to disease agents than operations growing birds to 8 to 10 weeks.
Nevertheless, NAE farms producing large birds have challenges of their own. On those operations, birds may outlive immunity acquired from the vaccines they get at an early age against Newcastle disease, infectious bursal disease, infectious bronchitis and reovirus. The result can be an increased susceptibility to the pathogens. The solution in most cases is a booster of vaccines for these diseases.
Seasonal impact
In warmer months, increased ventilation leads to lower coccidial pressure and better litter quality, so this is a good time for NAE producers to consider either vaccination or a bioshuttle program. Not every medication is suitable for year-round use, however. For example, nicarbazin is associated with heat stress, especially when administered at high dosages.2 It’s therefore important to limit its use to the cooler months.
At the other extreme is winter, when farms need to reduce air flow to save on energy costs, and flocks have higher exposure to disease agents. Wetter litter can also accelerate the sporulation of coccidial oocysts in the house and make flocks more susceptible to both coccidiosis and NE. For these reasons, it’s critical to ramp up control efforts and develop a long-term rotation strategy involving all available NAE tools.
Track and monitor
Although long-term planning for coccidiosis control is always a good idea, your program’s real-time effectiveness should be assessed routinely to make sure adjustments aren’t needed. Posting sessions as well as bird performance will be helpful in this regard. Coupling this information with historical data on necropsy results and flock performance for the past 1 or 2 years helps determine product efficacy and can be used to make better product choices.
One important reason real-time effectiveness should be monitored by routine necropsies is due to coccidial leakage, which occurs when some Eimeria oocysts survive flock treatment with non-ionophore anticoccidials. In conventional broiler flocks treated with ionophores, leakage leads to the development of immunity against coccidiosis in chickens. Leakage also occurs in NAE flocks treated with non-ionophore anticoccidials, but it’s turning out to be more difficult to manage. One exception may be zoalene, which is a non-ionophore anticoccidial that works similarly to an ionophore and can be a good choice for bio-shuttle programs.
The amount of leakage that occurs varies with products and their length of use. It’s taking the industry some time — as well as trial and error — to learn how to manage coccidial leakage in NAE flocks, but necropsies to monitor the intestinal status of birds can signal the need for intervention and remedial action.
Wrapping up
Much research is underway to explore the potential efficacy of alternative products for coccidiosis control, such as prebiotics, probiotics, oils and botanicals. Although some antibiotic alternatives have been shown to reduce coccidial-oocyst production, results in the field are inconsistent, and none has proved to be the “silver bullet” that NAE producers have sought. Research and field experience with the alternatives may lead to an effective way to control coccidia without medications, but such a development is unlikely in the immediate future.
For now, producers need to pick the right products based on cost and product performance to guard against losses, preserve what we have available for long-term use and avoid the need to make difficult ethical decisions regarding animal welfare.
Do not use zoalene in laying birds.
1 Da Costa M, et al. Effects of various anticoccidials as bio-shuttle alternatives for broilers under a necrotic enteritis challenge. 2017 Abstracts, International Poultry Scientific Forum. Atlanta, Georgia. M43, page 13.
2 Da Costa MJ, et al. Performance and anticoccidial effects of nicarbazin-fed broilers reared at standard or reduced environmental temperatures. Poult Sci. 2017 Jun 1;96(6):1615-1622.