By mid-August 1995, 55% of broiler embryos in North America were vaccinated for Marek's disease using the INOVOJECT system, with 201 INOVOJECT machines placed with 16 of the top 25 poultry producers, providing the industry with the capacity to inject in excess of 400 million eggs per month or about 5 billion eggs per annum. In ovo administration of a bursal disease antibody-infectious bursal disease virus (BDA-IBDV) complexed vaccine to specific-pathogen-free (SPF) embryos was safer and more potent than conventional IBDV vaccine alone because it delayed the appearance of bursal lesions, produced no early mortality, produced higher geometric mean antibody titers against IBDV, and generated protective immunity against challenge. In ovo administration of a BDA-IBDV complexed vaccine to broiler embryos generated antibody titers against IBDV sooner than conventional virus vaccinates, and generated protective immunity against challenge Direct DNA injection of plasmid DNA encoding beta-galactosidase into breast muscle in ovo and posthatch was an effective means to achieve both gene transfer and expression, with potential for the development of gene vaccines using plasmids encoding protective antigens from poultry pathogens. In ovo administration of 800 U chicken myelomonocytic growth factor (cMGF), a chicken hematopoietic cytokine for cells of the monocytic-granulocytic lineages, significantly reduced mortality associated with Escherichia coli exposure within the hatcher when compared to PBS controls (6.1 vs 12.4, P < or = 0.05), but not when compared to a yeast expression control. A procedure was developed enabling injection prior to the onset of incubation without compromising embryo viability. This in ovo injection process has opened up the window of embryo development during incubation for intervention, as illustrated by the 100% male phenotype produced in chicks hatching from eggs injected with aromatase inhibitor prior to incubation. These data illustrate some of the in ovo applications presently in use by the poultry industry, and under development or in research at EMBREX.

Young broiler chickens were fed from hatching until 3 weeks of age with a white corn-soy diet amended with varying amounts of lutein diester to supply 0, 5, 10, 20, 40, and 80 micrograms free lutein/g diet. The lutein diester was added as a stabilized, microencapsulated extract of marigold (Tagetes erecta) petals. The concentrations of lutein diester, lutein monoester, and lutein in the contents of the jejunum and large intestine and in serum, liver, and toe web from these birds were measured by high pressure liquid chromatography. The contents of the jejunum and large intestine contained a mixture of lutein diester, lutein monoester, and lutein. The serum contained lutein (approximately 90%), lutein monoester (approximately 10%), and traces of lutein diester. The liver contained the three carotenoid classes in ratios reflecting the serum ratios. The ratios in toe web, an integumentary depot site, were reversed with lutein diester much greater than lutein monoester greater than lutein. The concentrations of each class in each tissue bore a linear relationship to the concentration of lutein diester in the diet. A simple explanation for these data is that the dietary lutein diester was hydrolyzed mainly to lutein, which was absorbed through the intestinal wall into the blood stream where it was transported to the liver, a storage site, and to the integumentary sites where it is esterified to lutein diester which is the main depot form.

High performance liquid chromatography of yolks of hens fed a diet based on yellow corn, alfalfa, and soybeans revealed over 20 cartenoids. Lutein, lutein monester, lutein diester, 3'-oxolutein, cryptoxanthin, zeaxanthin, beta-carotene, and zeacarotene were identified by their retention times, visible absorption spectra, behavior on saponification, and their presence or absence when lutein was the primary carotenoid fed. Three weeks after placing the hens on a white corn-soy-based diet supplemented with lutein (20 micrograms/g diet), cryptoxanthin, zeaxanthin, and zeacarotene were undetectable in the yolk and lutein, lutein monoester, lutein diester, and 3'-oxolutein assumed new equilibrium concentrations. The data imply an esterification pathway and an oxidative pathway in laying hens for the metabolism of hydroxycarotenoids. Consideration of the concentrations and ratios of lutein and its metabolites in serum and yolk suggest a nonovarian site for the metabolism of lutein in laying hens.

The progression of changes in carotenoid metabolism during pale-bird syndrome caused by a coccidial infection was investigated. Male broiler chickens 15 days of age on a yellow corn and soybean meal-based diet were infected with Eimeria acervulina oocysts and their serum, liver, and toe webs were sampled at 0, 4, 6, and 10 days postinfection for HPLC analysis of carotenoids. At 4 days postinfection a drastic reduction (71%) in serum lutein, the main body carotenoid, and smaller reductions in liver (58%) and toe webs (38%) occurred. Derivative forms of lutein, mainly esters, continued to be lost from tissues for 10 days postinfection. These carotenoids were apparently lost via the intestinal tract because birds placed on a white corn and soybean meal-based diet at time of infection had lutein in their jejunal contents even at 7 days postinfection. The loss of carotenoids from the body was accompanied by a decreasing ability to absorb canthaxanthin, a red carotenoid, from the intestinal contents. The absorption of canthaxanthin measured at 0, 3, 4, 5, 6, and 7 days reached its low point of 1% of preinfection ability on Day 5 before a slow recovery commenced. Thus, the pale-bird syndrome caused by E. acervulina appeared to be the result of a loss of previously absorbed carotenoids coupled with drastic malabsorption of dietary carotenoids.

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