Twenty-four, 79-wk-old White Leghorn hens were assigned randomly to three diets containing 0, 2.5, or 5.0% conjugated linoleic acid (CLA). The diets were fed for 4 wk to determine the effect of dietary CLA on quality characteristics of eggs. Eggs were collected daily and stored at 4 C for 1, 7, 21, or 49 d. At the designated times, the eggs were processed to evaluate water content, fatty acid composition, color, proportions and pH of yolk and albumen. Firmness of yolk after the eggs were hard-cooked was also determined. The proportions of myristic, palmitic, stearic, CLA (9-cis, 11-trans CLA and 10-trans, 12-cis CLA isomers), and unidentified fatty acids in egg yolk lipids were increased as dietary CLA increased, but those of palmitoleic, oleic, linoleic, linolenic, arachidonic, and docosahexaenoic acid were decreased. Duration of refrigeration increased the proportion of egg yolk but decreased the contents of albumen and yolk lipids after 21 d or longer of storage. Egg yolk pH increased as refrigeration time increased, regardless of dietary treatment, but the increase was greater in the eggs produced by hens fed the CLA diets. Albumen pH increased significantly after 7 d of storage but remained unchanged until 21 d and then decreased by 49 d. Dietary CLA had no effect on the pH of albumen until 49 d of storage. After 49 d storage, egg albumen pH from hens fed CLA diets was lower than that of albumen from hens fed the control diet. Yolk color was not influenced by the dietary CLA and storage, but the egg yolk surface from hens fed CLA diets sometimes had relatively dark color with light spots. Dietary CLA and storage of CLA eggs increased the firmness of hard-cooked egg yolk. The texture of yolks from hard-cooked CLA eggs was rubbery and elastic, and the yolks were more difficult to break using an Instron. It was speculated that the quality changes of CLA eggs were related to the increase of yolk water content, the movement of ions between yolk and albumen through yolk membrane, and the changes of egg yolk pH during storage.

In the latter part of 1991 an unusual neurological disease was recognised on several farms in England. This report describes the case histories and clinical, biochemical and pathological findings in six calves and two lambs aged from two to 44 weeks obtained from five of these farms. Laminar cerebrocortical necrosis and severe bilateral necrosis of the thalamus and/or striatum progressing to cavitation were recognised in their brains. These changes are similar to those of experimental sulphate toxicity. Morbidity rates of 16 to 48 per cent and mortality rates of 0 to 8 per cent were recorded. The affected animals did not respond to vitamin B1 treatment; the erythrocyte transketolase levels of in-contact cattle and of one untreated affected calf and one untreated lamb were within the normal range. All five farms had recently introduced a proprietary concentrate ration containing ammonium bicarbonate. After this ration was withdrawn no new cases of nervous clinical disease were observed. It is suggested that, in at least some cases, the morphology and topography of lesions may distinguish sulphate induced polioencephalomalacia from that of sporadic thiamine-dependent cerebrocortical necrosis.

Two experiments were conducted to compare the dietary availability of P from meat and bone meal (MBM) with that of P from dicalcium phosphate (DP) for poults. Two batches of the same MBM were tested. The batches differed in fineness of grind; one was passed through a 10-mesh screen (openings of 2.03 mm) (MBM1O) and the other through a 12-mesh screen (openings of 1.91 mm) (MBM12). In Experiments 1 and 2, the low-P basal diets contained, by analysis, 0.54% P (0.2% nonphytate P) and 0.64% P (0.3% nonphytate P), respectively. Each batch of MBM and DP were included in isocaloric, equinitrogenous diets to obtain increments of 0.1, 0.2, 0.3, and 0.4% P added to the basal diet. Three pens, each containing seven poults, were assigned to each of the 13 dietary treatments. Poults were fed the diets from 5 to 11 and 6 to 13 d of age in Experiments 1 and 2, respectively. Regression analyses of the data showed that increases in BW and tibia ash were linearly related (P 0.05) from 100. Thus, the RA of P from MBM tested were equal to that of P from DP, and particle size of the MBM did not affect RA of P.

Two experiments were conducted to determine the effect of removing bacteria, including long segmented filamentous organisms (LSFO), from inoculum known to induce stunting syndrome (SS) in poults. Experiment 1 consisted of two identically designed trials. In each trial, each of four treatments was assigned to an isolator. Three treatments consisted of dosing, by crop intubation, groups of 1-day-old poults with unfiltered SS inoculum or filtrate of inoculum passed through .45- or .20-micron microfilters. Uninoculated poults were dosed with inoculum carrier, saline. Experiment 2 was done in battery facilities. Three rooms were used and each room housed one of three treatment groups. Triplicate pens of 10 poults each within each room were dosed by crop intubation with saline (uninoculated), unfiltered inoculum, or filtrate from .20-micron filtration. As compared with uninoculated poults, weight gain through 7 days was reduced 20% (P less than .05) by unfiltered and filtered inocula in both experiments. Jejunal maltase activity also was decreased (P less than .01) by unfiltered and filtered inocula. Feed efficiency (FE) was not determined in Experiment 1, but in Experiment 2, FE from 1 to 14 days of age was impaired by inoculum, irrespective of filtration. This effect was not evident during the 14- to 20-day period. The observation that the adverse effects of giving filtered inoculum to poults were the same as those caused by unfiltered inoculum indicated that bacteria, including LSFO, were not primary causative agents of the SS experimentally induced in poults.

Three experiments were conducted to determine the effects of supplementing practical diets of male turkeys with dl-alpha-tocopheryl acetate (TA). In Experiment 1, a factorial arrangement of dietary treatments [0, 12, 50, 150, and 300 IU TA/kg with 0 or 300 mg ascorbic acid (AA)/kg] was used. These 10 treatments were fed to poults from 1 to 41 d of age. From 41 to 118 d of age, the AA treatments were discontinued, and the 300 IU TA treatment groups were changed to 12 IU TA/kg. Neither TA nor AA treatments affected 41-d BW, feed to gain ratio (FE), or livability. No effects of dietary TA concentrations on turkey performance were observed through 118 d of age alpha-Tocopherol (TOC) concentrations of plasmas and livers were increased by increments of dietary TA, with substantial liver storage when toms were fed 150 IU TA/kg from 1 to 118 d. Supplementing diets with 0, 25, 50, 75, or 100 IU TA/ kg in Experiments 2 and 3 had no effect on performance of toms through 119 and 105 d, respectively. alpha-Tocopherol concentrations of plasma and red blood cells (RBC) increased linearly with increments of dietary TA. The same was true for livers in Experiment 2. Susceptibility of RBC to hemolysis induced by 400 microM t-butyl hydroperoxide (TBH) in Experiment 2 decreased with increasing dietary TA, and these decreases corresponded to increases in TOC concentration of RBC. However, the relationships between hemolysis and dietary TA or RBC TOC were inconsistent in Experiment 3 and varied according to concentration of TBH (200, 300, or 400 microM) and age of the toms. At 105 d of age, RBC of toms fed no supplemental TA were resistant to hemolysis, irrespective of dietary TA and TBH concentration. In Experiment 3, there were no indications of dietary TA effects on plasma peroxide concentration or activity of plasma creatine kinase. A positive relationship between dietary TA and blastogenic responses of blood lymphocytes was observed with concanavalin A when toms were at 44 d but not at 23 or 86 d of age. The overall data indicate that corn-soybean meal diets containing from 6 to 20 IU TOC/kg, but no supplemental TA supported satisfactory performance and well-being of male turkeys from 1 d of age to market ages when the turkeys were free of disease, as was true in the research reported here.