Given the recent and most welcome increase in the price of eggs, there is understandably a greater concern for shell quality to market as many eggs of acceptable quality as possible. The importance of shell quality is even greater with specialty products sold at a premium since losses are proportionately greater and the expectations of consumers are higher than with generic eggs.
Financial Impact of Shell Defects
It is calculated that a one million in-line operation with an average egg production of 80 percent would incur an annual loss of $25,000 for each 1 percent diversion of saleable eggs to breakers for each incremental 10-cent differential in revenue between wholesale and salvage values. Applying the basic formula, it is calculated that an average one million-hen complex could lose $225,000 annually with an additional 3 percent defects and a 30-cent/dozen difference between revenue from nest run and breaking. In the case of branded and specialty eggs, loss in goodwill, image, and consumer loyalty are difficult to quantify, but obviously are significant if an entire complex or a high proportion of flocks are affected.
Causes of Shell Defects
Nutrition - Traditionally, textbooks implicate improper diet as a major cause of shell defects. Deficiencies or imbalances in calcium and available phosphorous or inadequate intake of vitamin D3 are potentially responsible for osteomalacia in hens and reduced shell strength. Under commercial conditions in the United States, improper diet is seldom the cause of suboptimal shell mineralization. In the event that a pullet-rearing diet with 1 percent calcium content is inadvertently delivered to a flock in production, the turnover rate of feed in a house of over 60,000 hens with a 15-ton bin is generally so rapid that skeletal reserves of calcium are adequate to maintain shell quality with suboptimal calcium intake, providing the duration does not exceed a week.
Deficient feed as a result of improper formulation or mixing could be a consideration with diets prepared on site by specialty, organic or small-scale operations. A review of formulas, postmortem examination of hens, a survey of eggs and analyses of feed will usually identify the cause. Supplementing diets with excessive quantities of calcium, phosphorous or vitamin D3 will not improve shell quality if the defect is caused by other than a defective diet.
Appropriate preventive action is required for flocks, which may show defective shell density due to exposure to infectious bronchitis or adenovirus or on complexes where hens hyperventilate due to prolonged elevated temperature. Adding additional calcium to diets, in excess of a 4.5 percent level without balancing phosphorous and other nutrients is invariably counterproductive when the underlying cause for the decreased shell strength is unrelated to diet.
Elevated Ambient Temperature - Hens subjected to high temperatures hyperventilate, especially with concurrent elevated humidity or inadequate ventilation. An increase in respiratory rate is a physiological response to high temperatures to reduce body temperature by evaporation of moisture from the mucosa of the respiratory tract. Unfortunately, prolonged hyperventilation results in excessive excretion of carbon dioxide, resulting in respiratory alkalosis. This interferes with the active deposition of mineral in the shell gland of the oviduct, which depends on the activity of acid phosphatase.
Hens subjected to high temperatures during summer produce shells with reduced density. Checks may increase to 8 percent following a week during which house temperatures exceed 85 to 90° F for more than six hours per day. These episodes are usually associated with increased daily water intake exceeding six gallons per 100 hens and thermal distress noted by the high proportion of hens which pant together with decreased egg production and elevated mortality. Hens which have been dubbed are more susceptible to high ambient temperature than flocks with entire combs.
Basically, the only approach to resolving shell problems arising from high ambient temperature involves increasing ventilation rates to above 1 cfm/lb. live weight and applying evaporative cooling either through pads or a high efficiency nozzle system. These installations have the ability to reduce dry bulb house temperature by 10° F, depending on efficiency and prevailing humidity. In older houses, installation of new insulating material could be considered, but the cost effectiveness of this upgrade should be justified by improved egg production and shell quality. Nutritional approaches to resolving the problems of high temperature are generally ineffective and, at best, of short duration and ameliorative. Supplementing diets with vitamin C has been attempted in tropical and desert countries but the cost-effectiveness of the addition is questionable.
A number of years ago synthetic zeolites including sodium calcium aluminosilicate were promoted to improve shell quality based on limited trials. Generally, the industry has not adopted this measure to enhance shell quality under hot conditions.
Disease
Infectious Bronchitis - Exposure of flocks to infectious bronchitis (IB) during the late rearing stage will damage the oviduct tissue responsible for active deposition of mineral during shell formation. Flocks that are improperly protected by narrow spectrum vaccination during the early rearing period undergo exposure when transferred to multi-age in-line complexes. Variant strains of IBV that are responsible for defective shells have been identified in the Midwest and western states. Flocks that are exposed to IBV produce eggs with an abnormal shape, whorls of mineral especially at the equator of the egg and generally shells have suboptimal strength. The problem may be more pronounced towards the end of the first cycle and after molting.
Immunosuppression of flocks during the early brooding period following exposure to Marek's disease or infectious bursal disease (IBD) may reduce the antibody response to subsequent vaccination against IB and other antigens resulting in a mosaic of susceptibility in the flock. Detailed epidemiologic evaluation is indicated following recurring episodes of defective shell thickness and defects in successive flocks. This usually involves a structured serologic survey using ELISA to ascertain the antibody status of flocks at the time of transfer and at 20-week intervals thereafter in addition to the response to IBD and IB vaccinations. Since ELISA is group specific, the serum virus neutralization procedure is required to distinguish among IBV strains to which flocks may be exposed. It is imperative to select IB vaccines to protect flocks against field strains to which they may be exposed. Waning of immunity can be compensated by periodic "boosting" using an appropriate IB vaccine.
Even in immunocompetent flocks, a low level of protection can be caused by defective administration of vaccine. In evaluating the results of ELISA assays, it is necessary to establish that the geometric mean titer is consistent with protection. In addition, the range of ELISA titer groups should be reviewed to confirm uniformity in protection. Experience has revealed many flocks with a mean protective titer of 4,000 to 6,000 ELISA units but with up to 15 percent to 20 percent of individual hens in a sample of 20 sera showing susceptibility. Consecutive ELISA assays on wing-banded hens or samples obtained from identified cages should confirm seroconversion following exposure to IBV during the early stage of the first production cycle. Affected hens will continue to produce eggs with shells of suboptimal quality after challenge.
Respiratory Adenovirus - Adenoviruses are ubiquitous and if susceptible flocks are exposed during the production period, shell defects will occur. Generally, exposure to either respiratory adenovirus or IB results in a transitory decrease in the intensity of pigmentation in brown-shelled strains. Adenoviruses cause a reduction in shell density and a sandy texture at the poles of the shell. Checks can rise to above 10 percent for a two to three week period. Fortunately, pullet flocks are usually exposed to adenovirus during rearing due to inherent deficiencies in bio-security, resulting in flocks which are naturally immunized before transfer to laying houses.
Newcastle Disease - Newcastle disease (ND) can result in defective shells. Velogenic NDV strains are associated with rapidly rising severe mortality and respiratory or neural signs with virtual cessation of egg production. VVND together with exotic Highly Pathogenic Avian Influenza require rapid diagnostic intervention and control measures which are a federal responsibility. Lentogenic Newcastle Disease virus, which is ubiquitous, is seldom a cause of problems in the United States as flocks are generally well protected by vaccination and exposure to the mild virus during rearing.
Flock Age
Shell density will decrease with progressive age with obvious deterioration after 65 weeks. This is associated with increased egg volume and a concurrent decrease in the efficiency of active deposition of mineral nutrients into shell structure in the terminal part of the oviduct. Adequate nutrition with appropriate adjustment of calcium and available phosphorous levels, and control of ambient temperature, are more critical in older flocks than during the early phases of the production cycle. Recognizing the inherent problem of age-related deterioration, producers of specialty eggs discriminate against older hens and select flocks for production of eggs with acceptable quality.
Genetic Factors
The major primary breeders incorporate parameters associated with shell quality in their programs of index selection. Despite the emphasis on shell strength, some strains are more suitable for in-line breaking as they produce eggs with enhanced yield of solids and have shells with less desirable characteristics compared to competitive strains.
Shell Soiling
Generally, fly specks are removed by washing using commercial equipment operated in accordance with the manufacturer's recommendations. Specking should be resolved by suppression of fly breeding, which requires an integrated approach including frequent activation of manure belts, scraping manure boards, frequent flushing of lagoon systems or adequate ventilation of pits coupled with strategic use of insecticides and larvacides. Fecal staining is frequently encountered in old cages with sagging floors which reduces roll-out. Older cages are frequently associated with rust stains. If soiling cannot be removed by washing and if eggs with soiled shells are not eliminated by the dirt detector, consideration should be given to replacement of cages or conversion of an old house to a floor system.
A short-term and sudden increase in fecal staining may be associated with high ambient temperatures, causing hens to increase their intake of water with both diuresis (excessive urine production) and excretion of fluid feces. Restriction of water intake is counterproductive, especially since the basic cause is elevated temperatures and increased water intake is a necessary adaptive response. Adjustment of ventilation rate and activation of evaporative cooling, if installed, is required during summer months. Excessive fecal soiling may be due to increased salt intake and appropriate evaluation of formulations and analyses of diets should be carried out as accidental over-addition of salt is sometimes encountered. Feeding naturally contaminated limestone with high levels of magnesium sulfate will result in diarrhea. The problem is obviously complicated in cage systems where floors sag or if slope is less then 5 percent, inhibiting roll out onto the belts.
The Bottom Line
Shell defects can be costly in terms of diversion to breakers, store returns, goodwill and loss of brand image. Diligent diagnostic procedures are necessary to identify both primary and contributory causes of breakage in order to guide selection of appropriate corrective measures.
