White Leghorn pullets were fed standard laying rations supplemented with 0.0%, 0.05%, and 0.1% levels of dietary caffeine. There was no statistical difference in fertility among the three groups. Embryonic loss in eggs from pullets fed 0.05% caffeine was between values previously reported for 0.0% and 0.1% dietary caffeine. This suggests that embryonic mortality increases as levels of caffeine are increased in the diet up to 0.1%.
LUX (1954) has shown that the activity of sulfonamides against E. tenella was enhanced when used in combination with members of a class of pyrimidine and triazine compounds. Notable among these were
2,4-diaminopyrimidines. Joyner and Kendall (1955, 1956), Horton-Smith et al. (1960), Ball (1964) and Clarke (1962, 1964) not only confirmed the above reported findings, but expanded them to include
other Eimeria species. It is known today that sulfonamide-potentiator mixtures interfere with folic acid, dihydrofolic acid and tetrahydrofolic
acid metabolism in sequential biogenic fashion. The resulting beneficial therapeutic responses are the enhancement in activity,
lower drug concentrations, reduction in toxicity and nil drug resistance.
Mitrovic and Bauernfeind (1967) and Mitrovic (1967, 1968) have reported on sulfadimethoxine [(N’-(2,6-dimethoxy-4-pyrimidinyl)
sulfanilamide)]-anticoccidial and antibacterial activity in fowl when used alone. In evaluating the newly synthesized 2,4-diamino-5-substituted
benzylpyrimidines in combination with sulfadimethoxine against bacterial and protozoal laboratory infections, a high degree
of activity was exhibited . . .
Ro 5–0013 is a new broad spectrum coccidiostat and antibacterial containing sulfadimethoxine, N′-(2,6-dimethoxy-4-pyrimidinyl) sulfanilamide and potentiator, 2,4 diamino-5-(4,5-dimethoxy-2-methylbenzyl) pyrimidine, hereafter referred to as the potentiator, in a ratio of 5:3. Sulfadimethoxine alone has been reported to be highly effective, therapeutically, against all pathogenic species of coccidia in chickens (0.05%) and turkeys (0.025%) when administered in the drinking water (Mitrovic and Bauernfeind, 1967) and efficacious in the prevention of turkey coccidiosis at 0.0125% in the feed (Mitrovic, 1968). Mitrovic (1967) found that sulfadimethoxine was also effective in the therapy of fowl cholera in chickens (0.05%) and turkeys (0.025%) and infectious coryza in chickens (0.05%) when administered in the drinking water. Combining sulfadimethoxine and the potentiator, a folic acid antagonist, in a 5:3 ratio (Ro 5–0013) results in enhanced broad spectrum coccidiostatic and antibacterial activity when fed continuously to broilers at 0.02% and replacement birds at 0.01% (Mitrovic et al.,…
Lasalocid (.0125%) alone and combined with roxarsone (.005%) was evaluated for its effect on lesion reduction and oocyst suppression in thirty-five controlled replicated battery experiments, using in excess of 6200 broiler chickens. The chickens were inoculated with field isolates containing predominantly Eimeria tenella species.
Lasalocid (.0125%) used alone exhibited a high degree of anticoccidial activity.
Lasalocid (.0125%) fed in combination with roxarsone (.005%) showed, in addition to high anticoccidial activity, a further reduction in gross lesion (P<.01) and oocyst production (P<.05) over lasalocid used alone.
The ability of selected anticoccidial drugs to inhibit the colonization of day-old male broiler chicks (Cornish Rocks) by Escherichia coli 0157:H7, strain 932 was examined. Chicks were challenged with 1.8 × 10⁹E. coli 0157:H7 on Day 1, and fed diets supplemented with three selected anticoccidial drugs; monensin, nicarbazin, or robenidine. The cecal and colon fecal contents of the chicks were removed on Day 7, 14, and 21 postinoculation and examined for the concentration of E. coli 0157:H7 per gram of contents.
Monensin effectively reduced cecal and colon colonization of the chicks by E. coli 0157:H7. By Day 7, there were significant reductions in the bacterial population of the cecal contents of chicks receiving the monensin-medicated feed, and by Day 21 no E. coli 0157:H7 was recovered from the cecal and colon contents. The bacterial counts in the colon contents of the nicarbazin- and robenidine-medicated and unmedicated chicks were significantly higher than the monensin-treated chicks. Bacterial populations in the colon contents were high only when there were high bacterial concentrations in the cecal contents.
Control diets, and diets containing 4% 1,3-butanediol (BD), 8% BD, 4% 1,2-propanediol (PD) and 8% PD were offered ad libitum to broilers from 1 to 28 days of age. Body weight gain and feed intake were recorded, and plasma metabolites and liver glycogen were measured. When compared to the control diet, the synthetic compounds depressed (p less than 0.01) growth at the 4% level, but the effect was more pronounced (p less than 0.01) at the 8% level. The test compounds had no effect (p less than 0.05) on the efficiency of feed utilization. Four percent BD elevated (p less than 0.01) plasma beta-hydroxybutyrate and acetoacetate concentrations, and the ratio of beta-hydroxybutyrate to acetoacetate. The influence was more pronounced at the 8% level; PD did not affect (p greater than or equal to 0.05) ketone body concentrations. Neither BD, nor PD caused changes (p greater than or equal to) in plasma glucose, free fatty acids, cholesterol, or liver glycogen. Results are discussed with reference to feeding these compounds to monogastric and ruminant animals.
Five sources of corn distillers dried grains in the darkest DDGS source. Apparent and true lysine with solubles (DDGS), which varied in darkness of color, were collected from several processing plants in the Midwestern United States. Sources of DDGS were analyzed for their amino acid and energy contents, measured for color score, and evaluated for TMEn, apparent amino acid digestibility, and true amino acid digestibility. A precision-fed rooster assay was used, in which each DDGS sample was tube fed (25 g) to adult cecectomized roosters, and the excreta were collected for 48 h. The experiment was conducted as a randomized complete block design with 8 replicates. Seven adult roosters (averaging 75 wk of age) were used in each period, with 5 fed the DDGS sources and 2 fasted to estimate basal endogenous amino acid losses. One source (no. 5) was the darkest, 2 sources
Experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] will alleviate a cholecalciferol deficiency induced by low dietary cholecalciferol and no fluorescent lighting and to determine cholecalciferol requirements as influenced by fluorescent lighting or 1,25-(OH)2D3. In each study, nutritionally complete basal diets were fed to broiler cockerels from 1 to 16 d of age. Experiment 1 had a 2 x 2 x 2 factorial arrangement of treatments with 1,25-(OH)2D3 at 0 and 10 micrograms/kg, cholecalciferol at 2.75 and 27.5 micrograms/kg, and fluorescent lights on or off. Experiments 2 to 4 had four levels of dietary cholecalciferol (0, 5.0, 27.5, and 50.0 micrograms/kg) and fluorescent lights on or off (Experiment 2) or 1,25-(OH)2D3 at 0 and 10 micrograms/kg (Experiments 3 and 4). In Experiment 1, fluorescent lighting increased bone ash, and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and 0 microgram/kg 1,25-(OH)2D3 and reduced the severity of TD at both levels of cholecalciferol and 0 microgram/kg 1,25-(OH)2D3. In all cases 1,25-(OH)2D3 improved bone ash. The metabolite also decreased the incidence and severity of TD at both cholecalciferol levels with lights off and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and lights off. In the absence of fluorescent lighting and 1,25-(OH)2D3 27.5 micrograms/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Experiments 2, 3, and 4). However, even 50.0 micrograms/kg cholecalciferol was not as effective as fluorescent lights or 1,25-(OH)2D3 in reducing the incidence and severity of TD.
The effect was studied of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at various levels of vitamin D3, with adequate or inadequate dietary calcium, on performance and bone development in turkey poults. Two experiments were
conducted. Experiment 1 lasted 16 days and was a 4 × 2 factorial arrangement using a low calcium diet (.7%), with dietary
levels of vitamin D3 of 450, 900, 1,800, and 3,600 ICU/kg of diet and with or without 10 μg of dietary l,25-(OH)2D3. Experiment 2 lasted 14 wk and was a 2 × 2 × 2 factorial arrangement with vitamin D3 levels of 900 or 2,700 ICU/kg of diet, calcium levels at 58 or 100% of the National Research Council requirement (which varies
with age), and with or without 10 μg/kg of dietary l,25-(OH)2D3. In Experiment 1, increasing levels of vitamin D3 and l,25-(OH)2D3 supplementation significantly increased bone ash. Pairwise contrasts at specific vitamin D3 levels indicated that this effect of l,25-(OH)2D3 was greater at lower levels of vitamin D3. In Experiment 2, the 2,700-ICU level of vitamin D3 decreased the incidence of rickets at 3 wk and partially ameliorated a calcium deficiency, as indicated by an increase in
growth at the 2,700-ICU level of vitamin D3 in calcium-deficient diets from 8 to 14 wk. Vitamin D3 by calcium interactions on rickets at 14 wk of age and bone ash at 3 and 14 wk were similar and indicated also that vitamin
D3 partially ameliorated a calcium deficiency. In general, the addition to the diet of 1,25-(OH)2D3 increased bone ash and decreased the incidence of rickets in diets deficient in calcium but high in vitamin D3. There is very little evidence in the present study that indicates that 1,25-(OH)2D3 has any effect on tibial dyschondroplasia.
An experiment was conducted to determine the influence of adding 4 micrograms/kg of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] to the diet of 68-wk-old commercial egg production-type hens. The addition of the 1,25(OH)2D3 to the diet for 21 days resulted in significantly decreased egg production, egg weight, and feed consumption, and significantly increased plasma P, and bone-breaking load. Specific gravity of eggs, plasma Ca, tibia ash, and fertility and hatchability of eggs were not significantly affected by the addition of 1,25(OH)2D3 to the diet.
Bile Cu accumulation in Cu-depleted chicks fed Cu concentrations between .56 and 1.56 mg Cu/kg (0, .5, or 1 mg supplemental Cu/kg) was used to investigate the effect of microbial phytase at 600 U/kg and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at 10 micrograms/kg on Cu bioavailability from dehulled soybean meal (SBM) and cottonseed meal (CSM). The bioavailability of Cu (relative to CuSO4.5H2O, which was set at 100%) in SBM and CSM was 43 and 39%, respectively. Phytase addition (600 U/kg diet) decreased Cu bioavailability in SBM to 21%, but did not affect that in CSM (34%). Copper bioavailability in SBM was not affected by addition of 1,25-(OH)2D3 (10 micrograms/kg diet), but that in CSM was nearly doubled by 1,25-(OH)2D3 supplementation.
Two experiments were conducted to investigate the effects of supplementing a corn-soybean layer diet with either phytase, 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], or their combination. The basal diet was formulated to contain 3.00% Ca and 0.33% total P. In Experiment 1, 160, 56-wk-old laying hens were randomly assigned to treatment groups fed either the basal diet alone or diets supplemented with either 600 phytase units (FTU) per kilogram feed, 5 microg 1,25-(OH)2D3/kg feed, or their combination for an experimental period of 9 wk. Experiment 2 had the same design and treatment groups except that laying hens 24 wk of age were used for 8 wk. In both experiments, phytase had a positive effect on BW and increased plasma dialyzable P, tibia bone ash, and phytate P retention. In the first experiment, the addition of phytase, 1,25-(OH)2D3, or their combination prevented a rapid decrease in egg production due to a Mycoplasma gallisepticum infection observed in hens fed the basal diet. However, no benefit in egg production was obtained in the second experiment. No effects on egg weight and egg specific gravity were observed in both experiments. These results clearly indicate that phytase, and to a lesser extent 1,25-(OH)2D3, can be used to increase the utilization of phytate P by laying hens.
Studies were conducted to evaluate the level of dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] required to decrease the incidence of tibial dyschondroplasia (TD) in male broilers at 3 and 5 wk of age. The birds were reared in floor pens with wood shavings and fed a corn-soybean meal diet supplemented with 0, 3, 6, or 9 micrograms/kg 1,25-(OH)2D3. The diet contained, by averaged analyses, 0.73% calcium, 0.74% total phosphorus, and 0.22% phytate phosphorus. There was no treatment effect on body weight or gain: feed at either age. The incidence and severity of TD and the percentage of severe lesions were decreased and bone ash was increased by 6 micrograms/kg 1,25-(OH)2D3 at 3 wk of age. At 5 wk of age, the incidences of TD and severe lesions were decreased when 6 micrograms/kg 1,25-(OH)2D3 was fed. Bone ash was increased by this level in one of the two experiments. Plasma calcium was increased at 5 wk when 9 micrograms/kg 1,25-(OH)2D3 was fed, but there was no treatment effect on plasma dialyzable phosphorus or 1,25-(OH)2D3. The results indicate that 6 micrograms/kg 1,25-(OH)2D3 is effective for decreasing TD under practical rearing conditions.
Six hundred and sixty 75-wk-old Hy-line® W36 hens were allocated to one of three dietary levels of total phosphorus, .30, .60, or .90%. Birds were fed the diets for 3 days following which blood samples were collected at six different times, 2, 6, 10, 14, 18, and 22 h postoviposition (POP), and analyzed for 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3], total calcium (TCa), ionized calcium (Ca⁺⁺), percentage Ca⁺⁺ to TCa (%Ca⁺⁺/TCa), and phosphorus (P).
Plasma TCa and P significantly (P<.001 and .025, respectively) peaked at 10 to 14 h POP. The Ca⁺⁺ and %Ca⁺⁺/TCa significantly (P<.001) decreased during eggshell formation and following completion of the shell (22 h POP) levels returned to resting concentrations. Plasma 1,25-(OH)2 D3 results confirmed the existence and time of a circadian rhythm in laying hens. Peak concentrations of the metabolite occurred at 10 to 14 h POP, which resulted in a quadratic relationship (P<.001).
Plasma P decreased with decreasing dietary P and plasma 1,25-(OH)2 D3 increased (P<.025). Feeding low dietary P significantly (P<.001) increased Ca⁺⁺ and %Ca⁺⁺/TCa. Results of feeding various levels of dietary P to laying hens indicate that low P stimulates an increase in plasma 1,25-(OH)2 D3 as well as Ca⁺⁺ and %Ca⁺⁺/TCa, but high P actually suppressed this response.
Seventy-two-week-old Leghorn hens were fed a conventional corn-soybean meal diet, or comparable diets either devoid of all
supplemental vitamins, or with additions of 5 microg/kg 1,25-dihydroxycholecalciferol [1,25(OH)2D3], or 100 ppm vitamin C.
The diets were fed for up to 30 d, with periodic observation on bone characteristics of selected birds. With a vitamin-deficient
diet it took 30 d to realize significant reductions (P < 0.05) in bone breaking strength and these birds had less bone ash
as early as 15 d (P < 0.05), although bone calcium content was not affected. Adding 1,25(OH)2D3 to the diet caused an increase
in bone breaking strength after 15 d (P < 0.05) in the vitamin-deficient birds, although no difference was seen after 30 d.
This increase in bone strength was associated with increase in bone cross-sectional area. Vitamin C generally had little effect
on bone characteristics of the bird. These results suggest that there is little bone remodeling of older laying hens in response
to short-term feeding of 1,25(OH)2D3 or vitamin C.
A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol
(D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in
calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks
received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 μg/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate
(.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary
vitamin D3 levels well above the required amounts. The addition of 10 μg/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia
and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet
did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65
to 1.81%) and .73% phosphorus.
The research described in this paper relates the changes in serum concentration of calcium, phosphorus, and 1,25-dihydroxycholecalciferol [l,25(OH)2 D3] to changes in tibial ash percentage and the incidence of endochondral ossification defects (EOD) in flocks of commercially reared broiler chickens at 14 d of age.
Sequential studies of six Australian broiler flocks representing three major genetic lines were undertaken at weekly intervals from 1 to 28 d of age. Serum collected from birds was analyzed for total calcium, inorganic phosphorus, and l,25(OH)2 D3. Tibial ash percentage was also determined at weekly intervals, and the incidence of EOD was determined at 14 d of age by examining sagittal sections of the proximal tibiotarsus.
The EOD observed in the 14-d-old broiler chickens were characterized by enlarged zones of proliferating chondrocytes, similar to that which occurs during calcium- or vitamin D-dependent rickets. Three flocks had a 50% incidence of EOD at 14 d of age and were classified as severely affected. The other three flocks had incidences ranging from 12 to 16% and were classified as mildly affected.
Broiler flocks severely affected with EOD (50% incidence at Day 14) had lower (P ≤ .05) concentrations of l,25(OH)2 D3 than flocks mildly affected (12 to 16% incidence). Tibial ash percentages were lower (P ≤ .05) in the severely affected flocks between Days 14 to 28, and it is likely that a lower rate of ash accretion between Days 7 to 14 precedes the development of the EOD.
From these studies it is evident that flocks with a high incidence of EOD have significantly lower bone ash and 1,25 (OH)2 D3 compared with mildly affected flocks, and it seems probable that higher systemic concentrations of l,25(OH)2 D3 between 7 to 14 d of age will enhance the ability of broiler chickens to effectively mineralize the cartilaginous growth plates in the appendicular skeleton during early bone maturation.
Two experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] can prevent tibial dyschondroplasia in broiler chickens throughout the growing period when withdrawn from the grower diet. The birds were reared in floor pens with pine shavings to 6 wk in Experiment 1 and 5 wk of age in Experiment 2. Calcium was fed at .65 or 1.00% and 1,25-(OH)2D3 was fed at 0 or 5 micrograms/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2D3 were then fed 0 microgram/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschondroplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2D3 increased bone ash at both levels of calcium at 3 wk and the end of the experiments when supplemented for the duration of the studies. When 1,25-(OH)2D3 was fed, tibial dyschondroplasia was reduced in Experiment 2 only at 3 wk. Tibial dyschondroplasia was decreased at 5 wk in Experiment 2 when .65% calcium was fed with or without 1,25-(OH)2D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2D3 was decreased at 3 and 5 wk in Experiment 2 when 1.00% calcium was fed. The results of Experiment 2 suggest that 1,25-(OH)2D3 can prevent tibial dyschondroplasia caused by inadequate calcium when fed for only 3 wk. The bone ash observed when 1.00% dietary calcium is fed is equal to that obtained when 5 micrograms/kg 1,25-(OH)2D3 is fed with .65% calcium for the entire growout period.
Four experiments were conducted to study the effects of genetic strain, dietary Ca level, and feed withdrawal on growth, feed
efficiency, tibia bone ash, tibial dyschondroplasia (TD), and plasma 1,25-dihydroxycholecalciferol [l,25(OH)2D3] and 25-hydroxycholecalciferol [25(OH)D3]. Experiment 1 used five strains and Experiments 2 to 4 used three broiler strains. A TD-inducing basal diet was used in
each experiment. In Experiment 3, the birds were fed .60 or .95% dietary Ca, and in Experiment 4 the birds were fed the basal
diet and were fed or deprived of feed for 8 h daily. In Experiment 1, Athens-Canadian Randombred and Single Comb White Leghorn
chicks did not develop TD. In birds fed the basal diet alone, Peterson × Hubbard chicks had a significantly higher incidence
of the most severe TD lesion than two other broiler strains in each experiment and were significantly lighter in BW in two
of the four experiments. Of the three broiler strains, the incidence and average lesion score of TD was significantly higher
in Peterson × Hubbard birds in Experiment 2 and was numerically highest in the other three experiments. In birds fed the basal
diet, Peterson × Hubbard birds had significantly higher plasma l,25(OH)2D3 in two of the four experiments. Both feed deprivation and .95% Ca increased bone ash and decreased the incidence and severity
of TD. There were no significant differences in plasma l,25(OH)2D3 among strains of birds deprived of feed or fed .95% Ca. In three of the four experiments, high plasma l,25(OH)2D3 in Peterson × Hubbard birds was associated with an increase in the incidence and severity of TD.
Two experiments were conducted to compare the effects of supplementation with 1,25-dihydroxycholecalciferol [l,25-(OH)2D3] and a commercial phytase on P utilization by broiler males. Experiment 1 was conducted with three levels of total dietary
P (0.45, 0.55, and 0.65%) in corn-soybean meal diets supplemented with 5 μg/kg of l,25-(OH)2D3, 600 units/kg of phytase, or the combination of these supplements in a factorial arrangement from 0 to 21 d in battery brooders.
A second experiment was conducted with a similar design except that it was carried out in floor pens for a period of 35 d.
In Experiment 1, maximal BW was obtained at 0.65% P in chicks receiving the basal diet, 0.55% P in chicks receiving phytase
or l,25-(OH)2D3, and 0.45% P in chicks fed both supplements. Bone ash for chicks receiving the basal, phytase, l,25-(OH)2D3, and combination treatments at 0.45% total dietary P were 26.6, 34.9, 35.1, and 38.8%. There were significant interactions
between phytase and 1,25-(OH)2D3 for BW, bone ash, and incidence of rickets. Similar results were noticed in Experiment 2, with the exception that l,25-(OH)2D3 had little influence on BW from 0 to 3 wk, likely due to slightly higher dietary P. From 3 to 5 wk, BW and bone ash were
increased by each supplement and further increased by their combination. These interactions suggest different mechanisms of
action for these supplements in influencing phytate P utilization.
Three experiments were conducted to determine the effects of supplementing 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and a commercial phytase product on Ca and P requirements of 0- to 21-d-old broiler males. These experiments were conducted with four levels of dietary Ca and P in corn-soybean diets with and without supplementation of 5 micrograms/kg of 1,25-(OH)2D3, 600 units/kg of phytase, and the combination of these supplements. The results show that these levels of phytase and 1,25-(OH)2D3 can replace up to 0.1% of the inorganic P for criteria such as BW, bone ash, and plasma P. Both supplements increased phytate P retention, whereas higher levels of Ca and P decreased phytate P retention. The addition of 1,25-(OH)2D3, but not phytase, reduced Ca requirements and decreased the incidence of tibial dyschondroplasia. The combination of these levels of phytase and 1,25-(OH)2D3 replaced 0.2% inorganic P for criteria such as BW, bone ash, and P rickets. Total dietary P requirements are estimated to be between 0.55 and 0.60% at the levels of phytase and 1,25-(OH)2D3, listed above, or 0.45% when the combination is added. The Ca requirements are estimated to be 0.77% when 1,25-(OH)2D3 is added to the diet and 0.9 to 0.95% when phytase is added.
Three experiments were conducted to determine possible mechanisms involved in improving eggshell quality with sodium zeolite A (SZA) (trade name Ethacal® feed component), and cholecalciferol (vitamin D3) by studying the effect of dietary supplementation of SZA and vitamin D3 on plasma 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3], ionic calcium (Ca⁺⁺), normalized calcium (nCa⁺⁺), total calcium (TCa), percentage Ca⁺⁺ to TCa (PCa⁺⁺), pH, and phosphorus (P). In Experiment 1 (2 × 2 factorial arrangement of treatments), two levels of SZA (0 and .75%) and two levels of vitamin D3 (0 and 175 ICU/kg) were fed. In Experiment 2, five levels of vitamin D3 (100 to 500 ICU/kg) and two levels of SZA (0 and .75%) were fed using a 2 × 5 factorial arrangement of treatments. In Experiment 3, hens were fed two levels of SZA (0 and .75%). Blood samples were collected at 0 (Experiments 1, 2, and 3), 7, 14, and 21 h (Experiment 3) postoviposition (POP).
In Experiments 1 and 2, decreasing vitamin D3 decreased plasma l,25-(OH)2 D3 and P. Plasma TCa decreased when 0 ICU vitamin D3 was fed (Experiment 1), but was not affected by vitamin D3 level in Experiment 2. Supplemental SZA had no effect on plasma l,25-(OH)2 D3, TCa, or P in Experiments 1 and 2. In Experiment 3, plasma l,25-(OH)2 D3 and P peaked at 14 h POP, but Ca⁺⁺ was lowest at 14 h POP. Circadian rhythms for plasma l,25-(OH)2 D3, Ca⁺⁺, and P were not affected by SZA. There were no significant effects due to dietary SZA on plasma l,25-(OH)2 D3, TCa, Ca⁺⁺, PCa⁺⁺, nCa⁺⁺, pH, or P. It was concluded that SZA did not influence the synthesis of l,25-(OH)2 D3.
White Leghorn hens, age 34 wk, fed 0 to 3 μg/kg of 1,25 dihydroxycholecalciferol (1,25(OH)2D3) as the only source of dietary vitamin D3 with 2.5 or 3.5% calcium failed to achieve normal embryonic survival and hatchability of their fertile eggs. Improved egg
production was observed over a 24-wk period as the level of 1,25(OH)2D3 was increased. Eggs of hens fed the vitamin D-deficient diet showed significantly lower (P<.01) egg weight and shell strength
with a higher percent of soft shell eggs than those of hens fed l,25(OH)2D3 or vitamin D3. To study the possibility that l,25(OH)2D3 cannot be transferred into the egg yolk, yolks from the hens receiving varying levels of l,25(OH)2D3 and vitamin D3 were fed to day-old chicks. A standard vitamin D3 assay was developed and bone ash was determined on fat-free tibial bone. Significantly lower (P<.01) vitamin D activity per
gram of yolk was observed in yolks from hens fed 0 to 3 μg of l,25(OH)2D3 than in yolks of hens fed vitamin D3. These results demonstrate that insufficient 1,25(OH)2D3 is incorporated in the egg yolk to support normal embryonic survival and hatchability. This may be due to a decrease in available
receptor sites in the egg yolk or to the inability of l,25(OH)2D3 to cross the vitelline membrane.
Three experiments were conducted to examine the efficacy of dietary 1,25-dihydroxycholecalciferol [(1,25-(OH)2D3)] on the development of tibial dyschondroplasia (TD) in chickens divergently selected for high (HTD) and low (LTD) incidences of TD. In Experiment 1, chickens from the two lines were fed two calcium levels (0.75 and 1.0%), with and without 5 micrograms/ kg dietary 1,25-(OH)2D3. In Experiment 2, both lines were fed diets containing 1.0% calcium and 0, 5, 10, or 15 micrograms/kg 1,25-(OH)2D3. The addition of 1,25-(OH)2D3 did not reduce the overall incidence of TD in Experiment 1, but did reduce the incidence of severe TD from 69 to 48% in the chickens receiving the 0.75% calcium diet. In this experiment, LTD chickens had higher plasma phosphorus and bone ash. No line differences were noted between plasma vitamin D metabolites or intestinal vitamin D receptors. In Experiment 2, 5 micrograms/kg of 1,25-(OH)2D3 decreased the incidence of TD from 94 to 76% and number three scores from 69 to 44% (P < or = 0.001). Higher amounts of 1,25-(OH)2D3 further decreased TD, but there was a reduction in body weight above 5 micrograms/kg. Plasma 25-hydroxycholecalciferol [25-(OH)D3] and 1,25-(OH)2D3 were higher and intestinal vitamin D receptors were lower in HTD chickens than in LTD chickens. Plasma 1,25-(OH)2D3 was not affected by dietary treatment, but 25-(OH)D3 was reduced by dietary 1,25-(OH)2D3. Experiment 3 was conducted to examine effects of line and dietary 1,25-(OH)2D3 on plasma vitamin D metabolites and intestinal and growth plate receptors. No effect of genetic line or dietary 1,25-(OH)2D3 was observed for vitamin D receptors concentration or plasma 1,25-(OH)2D3 levels. Plasma 25-(OH)D3 was reduced when 1,25-(OH)2D3 was fed. These results indicate that HTD chickens are somewhat responsive to dietary 1,25-(OH)2D3, but this treatment failed to prevent the lesion in a large portion of the population.
Studies were conducted with corn-soybean meal diets to evaluate the effects of phytate phosphorus utilization on zinc absorption
and retention in broiler chicks. In the first two experiments, zinc-65 was used to determine zinc absorption. Experiment 1
was a 2 × 2 factorial with 0 or 5 μg/kg dihydroxycholecalciferol and 0 or 40 ppm supplemental zinc. In Experiment 2, 5 μg/kg
1,25-dihydroxycholecalciferol [l,25-(OH)2D3] or 750 units/kg phytase or both were added to a diet containing 35 ppm zinc. The diets in Experiment 3 were similar to Experiment
2 except that 600 units/kg phytase was fed. Experiment 4 was similar to Experiment 3 except that dietary phosphorus was decreased
by .15%. There were no treatment effects on body weight in Experiments 1 and 2. Zinc absorption was higher in zinc-deficient
birds in Experiment 1, but there were no other effects on zinc-65 absorption or retention. Body weight was increased by l,25-(OH)2D3 in Experiments 3 and 4 and by phytase in Experiment 4. Phytate phosphorus retention was increased by phytase and l,25-(OH)2D3 and was increased additively when both sources were fed. Dietary l,25-(OH)2D3 increased zinc retention at times during Experiments 3 and 4, but this response was inconsistent. Phytase did not affect
zinc retention. Phytase plus l,25-(OH)2D3 increased zinc retention synergistically in Experiment 3. Bone zinc was increased by l,25-(OH)2D3 and phytase, and there was an additive effect in Experiment 3. Plasma zinc and alkaline phosphatase were not affected. The
results suggest that supplemental zinc may be decreased in a corn-soybean meal diet when phytate phosphorus utilization is
Four hundred 53-wk-old Hyline W36 laying hens were randomly allocated to 10 treatments. The effects of feeding two vitamin
D3 metabolites, 1α-hydroxyvitamin D3 [1α-(OH) D3] and 1,25-dihydroxyvitamin D3 [1,25-(OH)2 D3 ], each at five dietary levels (0, .75, 1.50, 3.00, and 4.50 μg/kg of feed) were determined on eggshell quality and tibia
strength in commercial laying hens (Experiment 1). In Experiment 2, 1,440 Hyline W36 65-wk-old laying hens were used to determine
the effects of four levels of vitamin D3 (0, 500, 1,000, and 1,500 ICU vitamin D3/kg) and three levels of dietary 1,25-(OH)2 D3 (0, .5, and 1.0 μg/kg of feed) on eggshell quality, tibia strength, and egg production.
In Experiment 1, neither 1,25-(OH)2 D3 nor 1α-(OH) D3 affected eggshell quality or production criteria. Tibia weight was increased by adding either 1,25-(OH)2 D3 or 1α-(OH) D3. In Experiment 2, 1,25-(OH)2 D3 increased percentage of shell, shell weight, and egg breaking strength when 0 ICU D3/kg was fed but had no effect at higher levels of vitamin D3. Egg production, feed consumption, and egg weight were also increased with supplemental 1,25-(OH)2 D3 when 0 ICU D3/kg was fed. Tibia weight and tibia breaking strength were also increased by adding 1,25-(OH)2 D3 to the diet. The commercial laying hen metabolizes sufficient 1,25-(OH)2 D3 from dietary vitamin D3 to maintain shell quality but not enough to maintain tibia strength.
Three experiments were conducted to determine the influence of vitamin A on the utilization and amelioration of toxicity of cholecalciferol (vitamin D3), 25-hydroxycholecalciferol [25-(OH)D3], and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] in young broiler chicks. Two levels of vitamin A (1,500 and 45,000 IU/kg or 450 and 13,500 microg) were fed in all experiments. In Experiment 1, chicks were fed six levels of vitamin D3 (0, 5, 10, 20, 40, and 80 microg/kg). High dietary vitamin A decreased bone ash (P < 0.001), and increased the incidence of rickets (P < or = 0.02). Linear and quadratic responses to vitamin D3 levels were significant (P < 0.01) for body weight, bone ash, incidence and severity of rickets, and plasma calcium. In Experiment 2, six levels of 25-(OH)D3 (0, 5, 10, 20, 40, and 80 microg/kg) were added to the basal diet. Adding 25-(OH)D3 increased (P < 0.001) body weight, bone ash, and plasma calcium, and decreased rickets and plasma vitamin A. Adding 25-(OH)D3 overcame the reduction in bone ash produced by high dietary vitamin A showing a significant (P < 0.02) interaction. In Experiment 3, six levels of 1,25-(OH)2D3 (0, 2, 4, 8, 16, and 32 microg/kg) were added to the basal diet. High dietary vitamin A increased (P < 0.01) the incidence and severity of rickets. Adding 1,25-(OH)2D3 increased (P < 0.01) body weight, bone ash, plasma calcium, and reduced rickets and plasma and liver vitamin A. Adding 1,25-(OH)2D3 overcame the reduction in bone ash, and the increase in rickets produced by high vitamin A was significant (P < or = 0.05). These results indicate that high dietary vitamin A (45,000 IU/kg) interferes with the utilization of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3, increasing the requirement for each of them. Moreover, 45,000 IU/kg of dietary vitamin A ameliorated the potential toxic effects of feeding high levels of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3 to young broiler chickens. Further work is necessary to find the minimum levels of these vitamins needed to cause these effects.
This study investigated the protective effect of β-1,3/1,6-glucan on gut morphology, intestinal epithelial tight junctions,
and bacterial translocation of broiler chickens challenged with Salmonella enterica serovar Typhimurium. Ninety Salmonella-free Arbor Acre male broiler chickens were randomly divided into 3 groups: negative control group (NC), Salmonella Typhimurium-infected positive group (PC), and the Salmonella Typhimurium-infected group with dietary 100 mg/kg of β-1,3/1,6-glucan supplementation (T) to determine the effect of β-1,3/1,6-glucan
on intestinal barrier function. Salmonella Typhimurium challenge alone significantly decreased villus height (P < 0.001), villus height/crypt depth ratio (P < 0.05), and the number of goblet cells (P < 0.001) in the jejunum at 14 d postinfection (dpi), but significantly increased the number of intestinal secretory IgA (sIgA)-expressing
cells at 14 dpi (P < 0.01) and total sIgA levels in the jejunum at 7 (P < 0.05) and 14 dpi (P < 0.01) compared with the unchallenged birds (NC). Dietary β-1,3/1,6-glucan supplementation not only significantly increased
villus height, villus height/crypt depth ratio, and the number of goblet cells (P < 0.01), but also increased the number of sIgA-expressing cells (P < 0.05) and sIgA content in the jejunum at 14 dpi (P < 0.01) in birds challenged with Salmonella Typhimurium in comparison with Salmonella Typhimurium challenge alone. β-1,3/1,6-Glucan addition had significant inhibitory effects (P < 0.05) on cecal Salmonella colonization levels and liver Salmonella invasion of the Salmonella Typhimurium-infected birds compared with the PC group. Intestinal tight junction proteins claudin-1, claudin-4, and occludin
mRNA expression in the jejunum at 14 dpi was significantly decreased by Salmonella Typhimurium challenge alone (P < 0.01) compared with that of the NC group, whereas β-1,3/1,6-glucan supplementation significantly increased claudin-1 and
occludin mRNA expression (P < 0.01) at 14 dpi in the jejunum of the Salmonella Typhimurium-infected birds in comparison with the PC group. Our results indicate that dietary β-1,3/1,6-glucan can alleviate
intestinal mucosal barrier impairment in broiler chickens challenged with Salmonella Typhimurium.
A series of feeding trials lasting 21 days was conducted with Large White turkey poults to determine the effects of 0, 12.5, and 25% energy as 1,3-butylene glycol (BG) on growth and on both in vivo and in vitro lipogenesis. The substitution of 12.5 and 25% of the energy as BG and on both in vivo and in vitro lipogenesis. The substitution of 12.5 and 25% of the energy as BG depressed growth and feed efficiency of 21-day-old poults (P less than 01). The relative liver size was increased by BG (P less than .01) while liver lipid per 100 g of body weight was decreased (P less than .01) by BG. IN vivo lipogenesis, determined by the incorporation of tritiated water into liver fatty acids was decreased (P less than .05) by BG. The evolvement of CO2 from both (1-14C) acetate and from (U-14C) glucose was decreased by BG. The results of this study indicate that while lipogenesis can be decreased by BG, growth is also decreased. Therefore, the regulation of growth parallels the regulation of lipid synthesis in the turkey poult.
Salmonella enterica serovar Enteritidis is the major zoonotic and intracellular pathogen. Different strategies have been developed to prevent the S. Enteritidis infection. The beta-1,3-1,6-glucan of Schizophyllum commune was used as an immunological booster to determine the minimal dietary level of beta-glucan that would restrict S. Enteritidis infection through the effects of beta-glucan on the activity of macrophages and direct physical protection of the intestine. One-day-old male Single Comb White Leghorn chicks were used in all trials. In trials 1 and 2, the 0.1% beta-1,3-1,6-glucan treatment completely eliminated the viable S. Enteritidis from spleen and liver in an oral challenge of 10(8) S. Enteritidis without any harmful effect on BW, serum proteins, and immunoglobulin. Instead of a 21-d feeding period of beta-glucan, a 14-d treatment was enough to eliminate the S. Enteritidis in spleen and liver. In trial 3, an increase in the relative weight of bursa of Fabricius and phytohemagglutinin-P-inducing cutaneous basophil hypersensitivity was observed (P < 0.05). In trials 2, 3, and 4, the direct or indirect effect of beta-1,3-1,6-glucan on abdominal macrophages was examined. Sterilized 3% Sephadex G-50 was injected to induce abdominal (peritoneal) phagocytes in chicks fed with or without 0.1% beta-1,3-1,6-glucan. Significantly increased phagocytic and bactericidal capability to S. Enteritidis was found in abdominal macrophages either pretreated or in vitro treated with 0.1% beta-1,3-1,6-glucan. In conclusion, in addition to the physical properties to block S. Enteritidis entrance, 0.1% dietary beta-1,3-1,6-glucan may enhance the host defense to S. Enteritidis by directly upregulating the phagocytosis and bactericidal activity of abdominal macrophages in chicks.
The effect of diisopropyl 1,3-dithiolan-2-ylidenemalonate (NKK-100) on experimental fatty livers was investigated in chicks administered an antithyroid agent plus synthetic estrogen or in estrogenized, starved-refed chicks. NKK-100 was added at levels of 250, 500, 1000, and 1500 mg/kg diet. Liver weight was significantly decreased by administration of NKK-100 at 1500 mg/kg diet in the estrogen-administered chicks. Liver lipid content and liver lipid deposition were significantly and inversely decreased with increasing NKK-100 concentration in the diet in the estrogen administered chicks. Plasma transaminase activity, which was elevated by the estrogen administration, was reduced by the administration of NKK-100. These results suggest that NKK-100 may be of value in preventing fatty livers in poultry.
A synthetic energy source, 1,3-butanediol-1,3-dioctanoate (BDDO), and corn oil were fed at the 10% level in diets for chicks recovering from Newcastle disease virus at two levels of severity. There were little differences in plasma lipid concentrations between corn oil and BDDO groups. Liver lipid analyses showed significantly higher (P less than or equal to .01) triglyceride concentration for the BDDO group as compared with corn oil. In both trials, total liver lipid content was higher in all components for the BDDO group. Triglycerides and total lipids were notably lower (P less than or equal to .01) in skin of the BDDO group as compared with corn oil. Liver and skin lipid variations were attributed to different metabolic routes for BDDO and corn oil. The data suggest that BDDO tends to allow liver synthesis of triglycerides while suppressing lipid storage in the skin.
The development of antibiotic-resistant bacteria has led to a need for alternatives to antibiotics for growth promotion and disease prevention in poultry production. The helical polysaccharide beta-1,3/1,6-glucan is derived from the cell wall of Saccharomyces cervisiae and has immunomodulating activities. The objective of this study was to determine the ability of 2 supplementation programs with a commercial beta-1,3/1,6-glucan product to protect broiler chicks from experimental respiratory challenge with Escherichia coli. Chicks were housed in battery-brooders from 1 d of age and fed a standard starter diet or the same diet containing 20 g/ton (22 ppm) of purified beta-1,3/1,6-glucan either continuously (BG25d) or for only the first 7 d prior to challenge (BG7d). At d 7 one-half of the birds were inoculated in the thoracic air sac with 800 cfu of a serotype O2, nonmotile strain of E. coli. All surviving birds were necropsied at d 25. Body weight of survivors and feed conversion efficiency were protected from the adverse effects of E. coli challenge by BG7d but not by BG25d. Mortality was nominally decreased from 63% (control) to 53% in BG25d and 47% in BG7d, but these decreases were not significant. The relative weights of the liver and heart were increased, and the bursa of Fabricius relative weights were decreased by E. coli challenge, and these effects were modulated by beta-glucan treatment. Despite positive effects of BG7d in E. coli-challenged birds, the BW of nonchallenged birds was decreased by BG7d and BG25d. These results suggest that supplementation of broiler diets with beta-1,3/1,6-glucan may be valuable for decreasing production losses due to E. coli respiratory disease, but that the immune stimulation provided may also result in decreased production values under experimental battery conditions or for birds raised in an environment with minimal disease challenges.
Soybean meal (SBM) contains heat-resistant mannans. Domesticated turkeys are sensitive to mannans because of the high inclusion rate of SBM in their diets, causing increased chyme viscosity, wet droppings, and reduced feed conversion. Three experiments of similar design were conducted to determine the effect of mannan-endo-1,4-f'-mannosidase supplementation of corn-SBM diets on market turkeys. Experiment 1 was conducted at North Carolina State University using Nicholas hens raised from 1 to 98 d of age. Experiments 2 and 3 were conducted at PARC Institute Inc. using Large White turkey toms raised from 1 to 126 d of age. In each experiment, birds were randomly assigned to litter floor pens. Each pen was assigned to one of four experimental treatments in 2 x 2 factorial arrangement of two basal diets containing 44% CP and 48% CP SBM (SBM-44 and SBM-48, respectively) with or without 100 million units (MU) Hemicell/tonne (1 MU = 106 enzyme activity U). Birds fed SBM-44 had lower final BW (14.9 vs. 14.56 kg 18 wk BW / tom; 7.66 vs. 7.46 kg 14 wk BW/hen, P < 0.05) and higher final cumulative feed/gain than those fed the SBM-48. Hemicell supplementation generally improved performance of all birds, with a greater response in birds fed SBM-44. Hemicell improved BW and feed/gain by 1% (P = 0.779) and 3% (P = 0.377) in hens and 2.5% (P = 0.0016) and 4% (P = 0.0001) in toms, respectively. The results of these experiments indicate that some of the adverse effects of antinutritional factors of SBM of on turkey growth performance can be alleviated by dietary mannan-endo-1,4-beta-mannosidase supplementation.
Experiments were conducted to evaluate the potential for dietary 1,4-diaminobutane (putrescine) to influence eggshell quality and overall laying performance in hens. Forty-eight, 60-wk-old White Leghorn hens laying thin-shelled eggs were fed a corn and soybean meal-based diet supplemented with 0.00 (control), 0.05, 0.10, or 0.15% putrescine for 4 wk. Twelve hens that laid thick-shelled eggs were also fed the control diet. The feeding of supplemental putrescine decreased feed consumption; however, egg weight decreased only at higher levels of supplementation. Increasing dietary levels of putrescine responded quadratically in eggshell deformation, eggshell weight, and eggshell weight as a percentage of egg weight (P < 0.05). There were no significant differences in shell deformation, shell thickness, or shell weight when comparing hens laying thick-shelled eggs and those laying thin-shelled eggs that were fed 0.05% supplemental putrescine. Calcium intake, calcium retention, and calcium balance decreased linearly (P < 0.05) with increasing levels of dietary putrescine. Pancreatic putrescine concentrations were significantly higher (P < 0.05) in hens laying thick-shelled eggs compared with hens laying thin-shelled eggs. It appeared that pancreatic cells synthesized more polyamines in hens laying thick-shelled eggs. This increase in polyamines might have caused improved eggshell quality by increasing calcium transport. It was concluded that 0.05% supplemental putrescine improved eggshell quality; however, higher levels proved to be toxic.
An experiment was conducted to evaluate the potential dietary interaction between 1,4-diaminobutane (putrescine) and calcium on eggshell quality and overall laying performance. One hundred ninety-two 30-wk-old White Leghorn hens were fed a corn-and soybean-meal-based diet supplemented with 0.00, 0.05, 0.10, or 0.15% putrescine and 2.5, 3.0, 3.5, or 4.0% calcium in a factorial design (12 birds per diet) for 4 wk. The percentage of egg production increased linearly (P < 0.05) with increasing levels of dietary calcium. Significant interactions (P < 0.05) were observed between dietary putrescine and calcium for eggshell thickness, eggshell deformation, percentage of eggshell, calcium intake, total calcium retention, total eggshell calcium, and percentage of eggshell calcium. Interactions were due to quadratic effects of putrescine or calcium on these parameters. Eggshell thickness and percent eggshell increased when hens were fed 3.5% calcium in combination with 0.1% putrescine; however, calcium intake and calcium retention were significantly lower (P < 0.05). Eggshell quality improved with increasing dietary levels of calcium due to increased calcium retention and calcium balance. Increasing levels of dietary putrescine did not have a negative effect on eggshell quality; however, calcium intake was lower at higher-supplemented levels of putrescine. It was observed that dietary calcium in excess of requirements resulted in increased egg production and eggshell quality. Eggshell quality improved when hens were fed 3.5% calcium diet in combination with 0.10% putrescine. It was concluded that small supplements of dietary putrescine may improve eggshell quality, depending on dietary calcium concentration.
beta-1,4-Mannobiose (MNB) supplementation has been shown to prevent Salmonella Enteritidis infection in broilers by improving Salmonella Enteritidis clearance and increasing IgA production. This study examined in detail the gut immunomodulatory activity of MNB using microarray and real-time quantitative PCR analysis. One-day-old chicks were orally administered 0.1% (wt/wt) MNB 3 times a week for 28 d. Control birds received vehicle alone. Body weights and fecal IgA levels were monitored weekly. On d 28, spleen and bursa of Fabricius were removed and weights were recorded; samples of ileum, jejunum, cecum, spleen, thymus, and bursa of Fabricius were collected for histological examination; and ileum samples were collected for RNA extraction. No significant difference in BW or organ weights was observed between MNB-treated and untreated control birds, and no histological abnormalities were observed in any of the tissues examined. The MNB-treated chickens had significantly higher levels of fecal IgA over all 4 wk when compared with control birds. Microarray and reverse transcription PCR analysis revealed the upregulation of several genes involved in immune responses, including those involved in antigen recognition, processing and presentation (MHC class I and II), interferon-related genes, and genes involved in host defense. These results provide insight into the mechanism of action of dietary MNB in the intestine and confirm that MNB acts as a potent immune-modulating agent, exerting combined effects on the intestinal immune system.
The effect of EDTA on chicken liver D-fructose-l,6-diphosphate,1-phospho-hydrolase (FDPase) was investigated. The results indicate that a given concentration of EDTA can serve either as an activator or an inhibitor, depending on the relative concentration of Mg+ +. It was found that EDTA activated the enzyme only in the excess of Mg++ and that the enzyme activity would be completely inhibited whenever the concentration of EDTA was equal to or exceeded that of Mg+ +. It is suggested that the activation and the inhibition of this enzyme by EDTA are both mediated through the formation of chelate complex with Mg+ +.
1-Methyl-2-carbamoyloxymethyl-5-nitroimidazole.** has been reported by Peterson (1967 ,1968) and Whitmore et al. (1967, 1968) to be a compound of unusual potency against histomoniasis in experimental turkeys. In the trials conducted by the author, there appeared to be clinical benefit conferred in some treated groups in addition to the control of histomoniasis. Some of these birds became blind in one eye, and Arizona Paracolon 7: 1,7,8 was recovered from intraocular fluids. Trials were subsequently set up to test the efficacy of Ronidazole against Arizona 7: 1,7,8 in experimental poults.
MATERIALS AND METHODS
A culture of Arizona 7: 1,7,8 was passaged parenterally several times through chicks to enhance virulence. Broad Breasted White poults maintained in electrically-heated brooder batteries were medicated continuously with Ronidazole in the feed or water from day-old, and infected subcutaneously from the 10th to the 12th day with 0.1 ml. of a 24-hour broth culture of…
One of the prominent characteristics of Arizona paracolon is its persistence without a host. The Arizona group of organisms can survive in shady yards for at least six months (Worcester, 1965) and can remain infective contaminants for over six months in turkey yards (Rosenwald, 1965). Contaminated feed and water are among the routes of transmission of Arizona infection listed by Williams (1965). Since references to the persistence of Arizona paracolon in feed and water were not found in the literature, the following observations were considered worthy of reporting.
The culture of Arizona paracolon 7: 1,7,8 used in these studies was originally isolated from the shell of a soiled turkey egg. The inoculum for the feed and water was prepared by washing the growth from a 24-hr. tryptose agar culture with a sterile solution of 0.1% proteose peptone no. 3 and diluting the suspension to a reading of 55% light . . .
GENTAMICIN was isolated from members of the genus Micromonospora by Weinstein et al. (1963). This antibiotic was found effective in vitro against several species of Gram negative bacteria (Bulgar et al., 1963; Rubenis et al., 1964; Jao and Jackson, 1964). Gentamicin was subsequently found to be highly efficacious in vivo against species of Gram negative bacteria causing urinary tract infections in man (Jao and Jackson, 1964; Klein et al., 1964; Cox and Garvey, 1967; and Lipton, 1967).
Tests conducted in this laboratory by a method similar to that outlined by Tierno (1969), indicated that each of two isolates of Arizona 7:1,7,8 was inhibited in vitro by a gentamicin concentration between 0.625 and 1.25 micrograms per milliliter. Subsequently, a study was undertaken to determine the efficacy of gentamicin against artificially induced Arizona 7:1,7,8 infection in young turkeys. The manifestations of the “paracolon” infection have been described by Bruner and Peckham (1952),…
ROFENAID is the Hoffmann-LaRoche trademark for the compound containing sulfadimethoxine and ormetoprim in a 5:3 ratio. The efficacy of sulfadimethoxine against several species of chicken and turkey coccidia has been demonstrated (Mitrovic and Bauernfeind, 1967; Mitrovic, 1968). Mitrovic (1967) also reported the compound to be effective in preventing fowl cholera and infectious coryza in chickens.
Sulfadimethoxine in combination with ormetoprim was reported more effective against coccidiosis than sulfadimethoxine alone (Mitrovic et al., 1969b). This combination product (Rofenaid) was also found to be effective against some common bacterial infections in chickens (Mitrovic et al., 1969a). The present study was undertaken to evaluate the efficacy of Rofenaid against experimentally induced Arizona (paracolon) 7:1,7,8 (AR) and S. typhimurium infections in young turkeys.
MATERIALS AND METHODS
Five battery trials, each of four weeks duration, involving a total of 1500 poults of the Large, White type, were conducted. Fertile eggs were obtained from a commercial…
The turnover rate of plasma “low density fraction” (LDF, d < 1.006) lipoprotein was determined in two laying turkey hens.
LDF was labeled by injecting 1-14C-palmitate which was incorporated into the triglyceride (TG) of circulating LDF. The turnover
rates were determined from concentration and half life (t1/2) of the ultracentrifugally-isolated LDF. These values were 22 μ. equiv. of TG fatty acid (TGFA) per ml. plasma and 431 min.
The turnover rate of LDF was 17.57 mili equiv. TGFA/day or 5.0 g. of TGFA/day as stearate. It was estimated that 3.2 g. of
LDF-TGFA/day were removed as egg yolk.
Chicken embryonic adipofibroblasts (CEA) accumulate intracytoplasmic lipids when cultured in medium containing chicken serum
(CS), but not in medium with fetal bovine serum (FBS). To characterize this process of lipid accumulation, we evaluated the
expression of the enzyme glycerol-3-phosphate dehydrogenase (E.C.126.96.36.199) (GPDH), first in chicken tissues and then in CEA
cultured under diverse conditions. GPDH activity in adipose depots from 4-wk-old broiler chickens was similar or higher than
that shown by liver, the main organ for fatty acid synthesis in chickens, while skeletal muscle had the lowest levels of GPDH.
In vitro, GPDH activity increased in CEA cultured in the presence of CS but not in medium with FBS, paralleling the lipid
accumulation by these cells. Both lipid accumulation and GPDH activity were further increased in CEA cultured in the presence
of embryonic CS. Our results show that GPDH is highly expressed in avian tissues related to lipid metabolism and therefore
can be a reliable marker for avian adipogenesis, and suggest that ECS is an optimum source for the purification of avian adipogenic
Previous studies have demonstrated that Lactobacillus has anti-inflammatory properties, but the protective functions of Lactobacillus and mechanisms of inhibition of necrotic enteritis (NE) in the intestines of chickens have not been fully clarified. In the present study, we selected a probiotic strain, Lactobacillus fermentum 1.2029, which has good adhesive ability and a high survival rate in low pH and bile salts. The objective of this study was to examine the anti-inflammatory properties of L. fermentum 1.2029 against NE in chickens. Two hundred forty 1-d-old male Arbor Acres broilers were blocked into 3 experimental groups as follows: (I) nonchallenge control group, (II) Clostridium perfringens challenge group, and (III) C. perfringens challenge + L. fermentum 1.2029 group. Lactobacillus fermentum 1.2029 (1.0 mL/d, 10(8) cfu/mL) was orally administered daily to group III during the course of the experiment, and all uninfected control chickens were inoculated accordingly with the same volume of PBS. Clostridium perfringens (0.5 mL on d 1 and 1.0 mL on d 14 to 21, 10(8) cfu/mL) was administered to chickens in group II. At 28 d, scoring of gross NE lesions was performed. Ileal segments of approximately 2 cm from 24 chickens in each experimental group were collected and fixed in 4% (wt/vol) neutral-buffered formalin solution for histological scoring. Ileal mucosa samples were also collected for mRNA analysis by real-time PCR. The results showed that L. fermentum 1.2029 reduced the severity of NE lesions in chickens. Histological scores revealed that L. fermentum 1.2029 also reduced the inflammation damage of NE in chickens. Changes in cytokines and Toll-like receptors (TLR) were determined, and L. fermentum 1.2029 was found to increase interleukin-10 levels and reduce interferon-γ and TLR2 levels in NE-infected chickens. The results showed that L. fermentum 1.2029 was able to regulate the intestinal mucosal immune response and ameliorate inflammation by changing expression levels of cytokines and TLR.
This study examined the effects of stocking density on live performance, physiological stress level indicators, and processing yields of male broilers grown to 1.8 kg. A total of 3,120 Ross x Ross 708 male chicks was placed into 32 floor pens (5.57 m2/pen). Stocking density treatments were 25, (75 birds/pen), 30 (90 birds/ pen), 35 (105 birds/pen), and 40 (120 birds/pen) kg of BW/m2. The BW gain, feed consumption, and feed conversion were adversely affected with increasing stocking densities by 35 d. Physiological stress indicators (plasma corticosterone, glucose, cholesterol, total nitrites, and heterophil:lymphocyte) were not affected. Litter moisture was higher as stocking density increased, which led to higher footpad lesion scores. In parallel to growth responses, carcass weight was depressed by increasing stocking density, but carcass yield, absolute and relative amounts of abdominal fat, and carcass skin defects were not affected. Increasing stocking density decreased breast fillet weight and its relative yield and breast tender weight, but not breast tender yield. As calculated stocking density increased 5 kg of BW/m2 beyond 25 kg of BW/ m2, final BW and breast fillet weight decreased by 41 and 12 g, respectively. We conclude that increasing stocking density beyond 30 kg of BW/m2 adversely affects growth responses and meat yield of broilers grown to 1.8 kg but does not alter physiological stress indicators.
For a number of years, poultry selection has concentrated on growth velocity in meat lines, producing improvements in growth that have not been without consequence for muscle structure, metabolism, and meat quality. Higher growth rates may induce morphological abnormalities, induce larger fiber diameters and a higher proportion of glycolytic fibers, and a lower proteolytic potential in the muscles. After death, the faster development of rigor mortis increases the likelihood of paler color and reduced water holding capacity and poorer quality of further processed products. Reduced proteolytic potential is likely to increase toughness of poultry meats.
The present study investigated the potential of Salmonella enterica serovar Typhimurium (Salmonella Typhimurium) definitive type 104 (DT104) to contaminate eggs in vivo. Of 10 strains of Salmonella Typhimurium DT104, none caused egg contamination when hens were inoculated orally. Three passages of the strains through recovery from the reproductive organs of intravenously infected laying hens resulted in no egg contamination after oral infection of the hens. Feed and water withdrawal for 24 h at 5 and 10 d after oral infection with Salmonella Typhimurium DT104 slightly decreased egg production but did not lead to egg contamination. Finally, oral infection of pullets at the onset of lay (approximately 50% of egg production) resulted in egg contamination (1.7%) in 2 wk. In conclusion, the Salmonella Typhimurium DT104 strains used in the present study have a low possibility of causing egg contamination; however, because infection at the onset of lay can cause egg contamination, the introduction of Salmonella Typhimurium DT104 into the layer houses should be prevented, especially when hens start laying eggs.
Salmonella enteritidis and Salmonella typhimurium definitive type 104 (DT104) have been detected in the chicken oviduct, and their survival in egg albumen at the chicken body temperature of 42 degrees C may be important in oviductal and transovarian contamination of intact shell eggs. Eight S. enteritidis and 24 S. typhimurium DT104 strains were tested for their in vitro survival in egg albumen. The concentration of the organisms declined more rapidly when incubated at 42 degrees C than at 37 degrees C and dropped to nondetectable levels within 96 h at the higher, but not at the lower, temperature. In another experiment, 3 S. enteritidis and 3 S. typhimurium DT104 strains were randomly selected, and dosages of 20 and 200 cells of each strain were inoculated onto the vitelline membranes of egg yolks, which were then submerged in the original albumen and incubated for 24 h at 42 degrees C. Under these conditions, the organisms survived in albumen but did not penetrate the vitelline membrane. However, in a similar experiment, penetration did occur when the specimens were incubated at 30 degrees C for 72 h. The results suggest that low numbers of S. enteritidis and S. typhimurium DT104 can be expected to survive in egg albumen during the 24-h period of egg formation in the oviduct but would be unlikely to invade the yolk.before oviposition. However, depending on storage conditions following oviposition, S. enteritidis, as well as S. typhimurium DT104, could survive longer and may eventually invade the egg yolks.