Chick Edema Disease Syndrome in Young Turkey Poults

Two feeding bioassays were conducted to study the mortality pattern, incidence of edema and ascites formation and plasma composition of turkey poults fed diets containing varying levels of toxic fat (fat contaminated with polychlorinated dibenzo-p-dioxins) and/or salt. No significant changes in plasma concentrations of electrolyte and total protein and packed cell volume were observed in slaughtered poults fed diets containing toxic fat compared with poults fed a normal diet. However, a positive dose-response relationship between levels of dietary toxic fat (0,2 and 5%) and incidence of mortality with edema, ascites and hydropericardium was observed in poults fed diets containing 1% salt. The toxic effects of polychlorinated dibenzo-p-dioxins were accentuated by increasing the level of salt (0.5, 1 and 3%) in the diet. Mortality started at nine days of age and increased on days 10 and 11. The present experiments demonstrated that gross pathological changes similar to those reported for “chick edema disease” caused by feeding polychlorinated dibenzo-p-dioxins, could also be produced in young turkey poults. The etiology of the toxic effects of these organic compounds in edema formation is discussed.     

Tolerance of young turkey poults to various combinations of dietary furazolidone and salt.

Three feeding trials were conducted to study the tolerance of young turkey poults to furazolidone and to various combinations of salt and furazolidone in the diet. Poults of mixed sexes tolerated up to 0.03% dietary furazolidone from hatch to six weeks of age without harmful effects as judged from the data on mortality rate, feed intake, body weight and plasma composition. High mortality with cardiac dilation and ascites occurred in poults fed the same basal diet containing 0.05 or 0.07% furazolidone. Mortality was positively related to levels of dietary furazolidone, and occurred mainly between two and four weeks of age. The cumulative feed intake and body weight of these poults were significantly lower than those of the control poults at six weeks of age. There was indication of decreased renal function in poults on high furazolidone intake and the mechanism of furazolidone-induced cardiac dilation is discussed. Mortality rate, incidence of cardiac dilation with ascites and heart, liver and body weights and feed efficiency were similar in poults fed diets containing 0.022% furazolidone and varying levels of salts (0.5, 1.0 or 1.5%) compared with the control fed the same basal diet containing 0.5% salt from hatch to eight weeks of age. It is concluded that a starter diet containing 0.022% furazolidone and up to 1.5% salt does not affect the performance of poults from hatch to eight weeks of age.     

Effect of oral Escherichia coli inoculation on performance of young turkeys

A strain of Escherichia coli isolated from the yolk sac of stunted turkey poults was administered orally to day-old large white poults. Poults were inoculated with either 0.1 ml of sterile broth or 0.1 ml of a 10(-2) dilution of a 24-hr E. coli culture containing 3.4 x 10(8) viable bacteria per ml. Two levels of dietary protein (28 or 22%) were fed from 1 day to 3 weeks of age. Following E. coli inoculation of 3.4 x 10(5) viable bacteria at day one, body weight gain and feed consumption from 0 to 3 weeks of age were numerically increased 4.5 and 2.1%, respectively, and feed efficiency was significantly increased 2.4%. E. coli had a greater effect on performance of poults fed the 28% protein diet than on poults fed the 22% protein diet. Metabolism studies, conducted from 7 to 10 and from 17 to 20 days postinoculation, showed no significant changes in the measurements of nutrient utilization due to E. coli other than a 17% increase in nitrogen retention from 17 to 20 days by those poults fed the 28% protein diet.     

Pathogenicity of turkey coronavirus in turkeys and chickens

We designed this study to compare the replication potential of turkey coronavirus (TCV) and its effect in chickens and turkeys and to study the effect of singleand combined infection of turkey poults with TCV and astrovirus. We studied the pathogenicity of TCV in experimentally inoculated turkey poults and chickens by observing the dinical signs and gross lesions. Two trials were conducted with 1-day-old and 4-wk-old specific-pathogen-free turkey poults and chickens. One-day-old turkey poults developed diarrhea at 48 hr postinoculation. Poults euthanatized at 3, 5, and 7 days postinoculation had flaccid, pale, and thin-walled intestines with watery contents. The 4-wk-old turkeys had no clinical signs or gross lesions. One-day-old and 4-wk-old chicks developed no clinical signs or gross lesions although the TCV was detected in gut contents of the birds throughout the experimental period (14 days). In another experiment, mean plasma D-xylose concentrations in 3-day-old turkey poults inoculated with TCV, turkey astrovirus, or a combination of both viruses were significantly lower than in the uninoculated controls.     

Salt poisoning in turkey poults

A 4% mortality in 5-to-11-day-old turkey poults was attributed to 1.85% sodium chloride in the feed. The syndrome included peracute respiratory distress, ascites, and sudden death that resembled peracute heart failure. Clinical signs were observed only in the final phase of the toxicity, but progressive histologic lesions were found. Live, apparently unaffected poults showed increases in intracellular glycogen and cytoplasmic granularity, loss of striation, and early mild intercellular myocardial edema; similar but more severe histologic lesions were seen in live, ascites-affected poults. The ascites-affected poults had hydropericardium and hydrothorax which seemed to develop just minutes before death. Ultrastructurally, focal areas of myocardial cells exhibited myofibrillar disarray, lysis of myofilaments, widened Z-bands, and dilation of sarcoplasmic reticulum.     

Effect of Dietary Lactose on the Productive Performance of Young Turkeys

Studies were conducted to assess the performance of turkeys fed diets containing lactose. Study 1 consisted of 96, mixed-sex turkey poults that were housed in battery cages and fed diets containing 0 (8% cornstarch), 0.5, 1, 2, 4, or 8% lactose from 0 to 6 wk. Study 2 used 360, mixed-sex turkey poults that were raised in floor pens and fed a commercial diet and diets containing 0 (4% starch), 0.5, 1, 2, or 4% lactose from 0 to 6 wk. Diets and water were offered ad libitum throughout both trials. The objectives were 1) to determine the effect of lactose on turkey performance and 2) to establish the optimum level for lactose inclusion in diets. In Study 1, feed intake, BW, fecal ammonia and nitrogen, and feed efficiency were determined. Diet composition, BW, feed intake, total body and carcass composition, cecal pH, volatile fatty acids (VFA) and lactic acid were measured in Study 2. Turkeys consuming the 4% lactose diet gained the most weight (P < 0.01) compared with other treatments in Study 1, and lactose improved feed efficiency. In Study 2, all lactose diets resulted in heavier BW (P < 0.05) compared with the commercial diet. Turkeys consuming diets with 0.5, 1, 2 or 4% lactose had less total body fat compared with turkeys consuming a commercial or 0% lactose diet (P < 0.05).     

Influence of selenium on aflatoxin B1 or crotalaria toxicity in turkey poults

This research compared the toxic effects of aflatoxin B1 and monocrotaline, the active principle of Crotalaria spectabilis, and the additive effect between aflatoxin B1 and monocrotaline in turkey poults. It was of interest whether selenium fed at dosage levels of 0.1, 5, or 10 micrograms/g of feed would protect against the toxic effect of aflatoxin and/or monocrotaline, and whether the toxicants would result in detectable residues in poult tissues. A total of 180 healthy 1-day-old male turkey poults was assigned at random to 12 treatment groups (15 birds/group). Body and liver weight losses, and low serum concentrations in total protein (TP), albumin (A), alpha-globulin (alpha G), and beta-globulin (beta G), as well as high values in gamma-globulin (gamma G), were produced in the groups fed crotalaria. Pathologic changes were induced by monocrotaline with no protection afforded by the added selenium. Low values in TP, A, alpha G, and beta G and in body and liver weights were observed in groups given the combination of aflatoxin plus crotalaria. Gross lesions were associated with an additive toxic effect and a lack of protective effect of selenium against this combination. However, higher values in TP, A, alpha G, and beta G, and liver weights in groups fed aflatoxin B1 plus selenium indicated that selenium had a protective effect against aflatoxin toxicity. Residues of aflatoxin B1 and aflatoxin M1 were found in the kidneys of poults fed aflatoxin B1; also, dehydroretronecine (the metabolite of monocrotaline) was detected in livers of poults fed Crotalaria spectabilis seeds.     

Supplementary biotin decreases tibial bone weight,density and strength in riboflavin-deficient starter diets for turkey poults

1. Growth and skeletal responses to different dietary concentrations of riboflavin and biotin were compared in turkey poults from hatch to 21 d of age. The birds were fed on a turkey starter diet with different concentrations of supplementary riboflavin (0, 20 and 40 mg/kg) and biotin (0, 0.3 and 0.6 mg/kg) in a factorial design.

2. Poults fed on diets with no supplementary riboflavin had poor gait scores, decreased times to sit and higher rates of culling compared to poults fed on the control diet (20 mg biotin and 0.3 mg riboflavin/kg diet). Histologically, riboflavin deficiency was associated with a peripheral neuropathy similar to that described previously in chicks and, unexpectedly, in growth plate abnormalities.

3. Tibiae of poults fed on the control diet were larger, more dense, stronger and stiffer than the diets with no supplementary riboflavin.

4. Increasing supplementary biotin in poults fed on diets with no supplementary riboflavin was associated with a decrease in tibia weight, density, strength and stiffness.

5. The results demonstrated that riboflavin deficiency in fast-growing turkey poults was associated with growth retardation, growth plate disturbance and peripheral nerve dysfunction leading to an inability to walk.     

Pathology of vitamin D deficiency in growing turkeys

Turkey poults were fed a vitamin D-deficient diet and examined for clinical signs and structural changes of bone and parathyroid glands. Vitamin D-deficient poults developed ricketic changes during days 10 to 14. Control poults (deficient diet plus vitamin D) did not develop rickets. In deficient poults, lengths of proliferating-prehypertrophied zones of growth plates increased significantly in the proximal tibiotarsus but were only slightly elongated in the distal tibiotarsus. Unmineralized hypertrophic chondrocyte zones increased in length rapidly in conjunction with a decrease in the length of mineralized hypertrophic degenerative zones; this occurred more rapidly in proximal than in distal tibiotarsus. Other ricketic changes included decreases in bone ash, total femoral bone ash (calcium, phosphorus, magnesium), bone length, and body weight. Plasma alkaline phosphatase was increased, calcium was normal, and phosphorus was normal or elevated. Parathyroids were hyperplastic and had foci of degeneration. Vitamin D3 metabolites 25OHD3, 1,25(OH)2D3, and 24,25(OH)2D3 were rapidly depleted. Increase in bone ash Ca/P ratios in deficient poults suggests that phosphorus may be selectively released from ricketic bone. Low 25OHD3 and 1,25(OH)2D3 of control poults early in the experiment suggests that 1,400 IU of vitamin D3/kg of feed may not be an adequate level of vitamin D3 for growing turkey poults.     

The susceptibility of young chickens, ducks, and turkeys to the photosensitizing effect of Ammi visnaga seeds.

Young chickens, ducks, and turkeys were exposed to sunlight and fed various amounts of Ammi visnaga seeds for 14 days in an attempt to induce photosensitization. In chickens, seeds at 1.25% in the diet had no effect whereas 3% induced mild signs of photosensitization within 6 to 8 days. No visible effects resulted in ducklings from 1.5, 3 and 6% in the diet, or in turkey poults from 3%. These differences appear to be due to differences between these avian species in the metabolism of the photodynamic agent.     

Pathogenicity of embryo-adapted serotype 2 OH strain of infectious bursal disease virus in chickens and turkeys

The pathogenicity of serotype 2 OH strain of infectious bursal disease virus (IBDV) to specific-pathogen-free (SPF) chicken embryos and 2-wk-old SPF chickens and turkey poults was investigated. The virus was pathogenic for chicken embryos after five passages as evidenced by pathologic changes in inoculated embryos. The embryo-adapted virus was not pathogenic for 2-wk-old SPF chickens and turkey poults as indicated by lack of clinical signs, gross or microscopic lesions in the bursa of Fabricius of inoculated birds. Bursa-to-body-weight ratios of the inoculated chickens and turkey poults were not significantly different from those of uninoculated controls. Virus-neutralizing antibodies to serotype 2 IBDV were detected in inoculated chickens and turkeys. Results of this study indicated that the embryo-adapted serotype 2 OH IBDV isolate that is pathogenic for chicken embryos is infectious but not pathogenic in chickens and turkeys.     

Rickets in turkey poults

Fifteen outbreaks of rickets were diagnosed in turkey poults in Saskatchewan between 1978 and 1981. No relationship to farm, source of poults, or source of feed was apparent. Most outbreaks started when the poults were between 10 and 14 days of age, and they had recovered by 28 days of age. Losses varied from 1% to 14% of poults started. Skeletal lesions were characteristic of a vitamin D or calcium deficiency. On the basis of chemical analyses, adequate levels of calcium and phosphorus and proper amounts of vitamin premixes were present in the feed, but in five outbreaks biological feed tests implicated feed as a causative factor. The severity of rickets in poults fed defective feeds was markedly reduced by providing the poults with extra vitamin D in the drinking water or by injection. Two premixes used in different feeds contained adequate available vitamin D on the basis of biological testing. In some of the outbreaks, the rickets may have resulted from inadequate distribution of vitamin D in the feed, destruction of vitamin D during feed processing, or some unknown factor in the feed interfering with vitamin D utilization.     

Effect of hypoxia and diet on spontaneous turkey cardiomyopathy (round-heart disease).

The purpose of this study was to examine the effect of hypoxia-induced hypoxemia and rate of growth on spontaneous dilatory cardiomyopathy in turkey poults. Turkey poults grown in a hypobaric chamber at an atmospheric pressure of 592 mmHg (calculated partial pressure of oxygen: 124 mmHg; calculated altitude and O2 equivalents: 2054 m and 16.3%) on a rapid-growth diet developed a mainly right ventricular dilatory cardiomyopathy typical of the acute form of spontaneous turkey cardiomyopathy (STC). Poults grown in a hypobaric chamber on a slow-growth diet had a much lower incidence of STC. Control poults at atmospheric pressure, altitude 295 m (calculated atmospheric pressure: 735 mmHg; partial pressure of oxygen: 154 mmHg, 20.26% O2), on a rapid-growth diet had an incidence of STC similar to that of the slow-growth hypobaric group, while those on a slow-growth diet had a lower incidence.     

The effects of probiotic and mannanoligosaccharide on some haematological and immunological parameters in turkeys

The study was conducted to investigate the effects of mannanoligosaccharide (MOS) and probiotic supplementation on haematological and immunological parameters in turkeys. A total of 72, 15-day-old white hybrid converter turkey poults were used in this study. Poults were assigned into three groups, each group consisted of six poults and the trial was repeated four times. The control group was fed a basal diet without supplemented probiotic and MOS, and treatment groups were fed either 1 g/kg MOS or probiotic added diets. At the end of the 15-week treatment period, samples of blood were collected to determine immunological and haematological values. The comparison among the groups showed that both the probiotic and MOS supplementation resulted in significant increases (P < 0.05) in the serum IgG and IgM levels, and significant decreases (P < 0.05) in the peripheral blood T lymphocyte percentage compared with those of the control group. Mean serum IgG level (7.06 g/l) was significantly higher (P < 0.05) in poults supplemented with probiotic compared with MOS (6.76 g/l). It was observed that the probiotic supplementation caused statistically significant increases (P < 0.05) in the erythrocyte count, haemoglobin concentration and haematocrit values, but MOS supplementation did not have a significant effect (P > 0.05) on these parameters. Total leucocyte and differential leucocyte counts were not affected by dietary MOS and probiotic supplementation. These results show that MOS or probiotic may elevate IgG and IgM levels in turkey. The MOS and probiotic that enhance immunoglobulin levels will have a more positive effect on growth performance, production and turkeys' ability to resist disease.     

Poliomyelomalacia, pancreatic necrosis, and cerebellar malacia in turkey poults

Two-to-5-week-old turkey poults from three large Minnesota flocks exhibited ataxia, flaccid paralysis, and up to 5% mortality as unexpected death. The major post-mortem finding was cerebellar hemorrhage and softening detected in 22 of 89 clinically affected poults. Histologic findings were severe focal or multifocal poliomyelomalacia in the lumbosacral intumescentia of the spinal cord, cerebellar malacia, and single-cell or multifocal coagulative necrosis of pancreatic acinar cells. Thirty of 32 clinically affected poults examined had microscopic spinal cord lesions, 12 of 48 had cerebellar lesions, and 26 of 47 had pancreatic lesions. Gross and microscopic cerebellar lesions resembled those of vitamin E deficiency in chicks. Hepatic selenium levels were approximately twice normal expected levels for poults.     

Ulcerative cholecystitis produced by 3-nitro-4-hydroxy-phenylarsonic acid toxicosis in turkey poults

Naturally occurring ulcerative cholecystitis was present in a flock of 21-day-old turkey hens that were accidentally given at least 0.004% 3-nitro-4-hydroxy-phenylarsonic acid (3-NITRO) in their water for 2 days. Similar lesions were reproduced by administering 0.002% 3-NITRO to 2-day-old turkey poults for 6 days. Turkeys 31 days old were given up to 0.004% 3-NITRO in their water for 6 days, but no gall bladder ulcers were present in these poults. The toxicity to turkeys of 3-NITRO in the water appears to be age-dependent.     

The effect of a direct-fed microbial (Primalac) on turkey live performance

Two pen trials and 2 field trials were conducted to determine whether a direct-fed microbial (DFM; Primalac) was effective in improving turkey productive performance. In the pen trials, typical turkey diets were formulated with and without Primalac. All feed was provided by a commercial feed mill. In trial 1, Large White male turkey poults were placed in 48 pens (18 birds/pen, 24 pens/treatment) on the day of hatch and were reared to 20 wk. In trial 2, Large White female turkey poults were placed in 48 pens (30 birds/pen, 24 pens/treatment) on the day of hatch and were reared to 18 wk. Cumulative FCR was significantly improved for birds fed DFM feed compared with birds fed control feed at 20 wk in trial 1 and at 8 wk in trial 2. Body weight was significantly greater for birds fed DFM feed compared with birds fed the control feed through 12 wk in both trials. In 2 field trials, 2 brooder houses and 4 grow-out houses were paired on each farm (4 brooder houses and 8 grow-out houses total). All birds received the same feed provided by the integrator. The DFM was provided in the water from placement to market in 1 brooder house and in the 2 matching grow-out houses. Breeder flocks were equally represented in both brooder houses within each trial. Approximately 12,000 male poults were placed in each brooder house and were transferred to 2 grow-out houses at 5 wk. Although no statistical analyses were computed for the field trials, there was a nominal improvement in performance associated with the DFM: mean livability was increased by 3.5%, mean BW was increased by 0.9 kg (2 lb), mean total weight removed from the farms was increased by 13,706 kg (30,153 lb), mean FCR was improved by 0.165, and cost of production was reduced by $0.0195/kg ($0.043/lb) of BW by the DFM. In conclusion, the DFM product (Primalac) used in these studies was effective in improving turkey live performance.     

Infectious bursal disease virus and Alcaligenes faecalis infections in turkeys

To determine if infectious bursal disease virus (IBDV) augments alcaligenes rhinotracheitis (ART), turkey poults were exposed to IBDV, Alcaligenes faecalis, or both IBDV and A. faecalis. In five experiments, poults exposed to IBDV alone exhibited neither signs of disease nor histopathologic lesions. Serum antibodies to IBDV were detected in poults exposed to this virus by inoculation and by direct contact with inoculated birds. Signs of ART were observed 4 to 6 days following exposure to A. faecalis. Clinical signs of ART and histopathologic lesions in the upper respiratory tract of poults exposed to both IBDV and A. faecalis were similar to those observed in poults exposed to A. faecalis alone.