In vitro and in vivo efficacy of a hydrated sodium calcium aluminosilicate to bind and reduce aflatoxin residues in tissues of broiler chicks fed aflatoxin B1.

The aim of this study was to determine the binding capacity of a hydrated sodium calcium aluminosilicate (HSCAS) for aflatoxin B(1) (AFB(1)), and the efficacy of the HSCAS to reduce the concentrations of residual AFB(1) and its metabolites in the liver and kidney of broilers fed AFB(1). One hundred 1-d-old male broilers (Ross 708) were maintained in chick batteries and allowed ad libitum access to feed and water. A completely randomized design was used with 5 replicate pens of 5 chicks assigned to each of 4 dietary treatments from hatch to 21 d. Dietary treatments included the following: A) basal diet (BD), with no HSCAS or AFB(1), B) BD supplemented with 0.5% HSCAS only, C) BD supplemented with 2.5 mg of AFB(1)/kg of feed, and D) BD supplemented with 2.5 mg of AFB(1)/kg of feed and 0.5% HSCAS. On d 21, 5 chicks from each treatment were anesthetized with carbon dioxide, killed by cervical dislocation, and samples of liver and kidney were collected for analysis of AFB(1) residues. The percentage of AFB(1) bound for each concentration of adsorbent (100, 10, 1, 0.5, 0.25, and 0.05 mg/10 mL) was 100, 91.1, 81.8, 75.4, 40.1, and 8.8%, respectively. Concentrations of aflatoxin residues (AFB(1), aflatoxicol, aflatoxins B(2) and G(1)) were lower (P < 0.05) in livers and kidneys of birds fed AFB(1) plus HSCAS (diet D), when compared with birds fed AFB(1) alone (diet C). However, histopathology data from the in vivo study indicated that HSCAS did not prevent lesions associated with aflatoxicosis. The decrease in the bioavailability of AFB(1) caused by the HSCAS reduced aflatoxin residues in liver and kidney, but not enough to completely prevent the toxic effects of AFB(1) in broilers.

Effects of melamine in young broiler chicks.

A study was conducted to determine the toxicity of melamine in young broilers fed graded levels of melamine. An additional objective was to determine melamine residual levels in selected tissues. One hundred and seventy-five 1-d-old male Ross broiler chicks were sorted to a randomized block design in stainless steel battery pens. Chicks were assigned to 7 dietary treatments containing 0, 0.5, 1.0, 1.5, 2.0, 2.5, and 3.0% melamine. Each dietary treatment was fed to 5 replicate pens of 5 chicks for 21 d. Mortality increased quadratically (P<0.001) with increasing dietary concentrations of melamine. However, compared with controls, mortality was only higher (P<0.001) in birds fed≥2.5% melamine. Feed intake decreased linearly (P<0.001), whereas BW gain decreased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, both feed intake and BW gain were lower (P<0.001) only in birds fed≥1.0% melamine. Relative kidney weights increased linearly (P<0.001), whereas relative liver weights increased quadratically (P<0.05) with increasing dietary concentrations of melamine. Melamine residues in breast muscle and liver tissue increased linearly (P<0.001) with increasing dietary concentrations of melamine, whereas melamine residues in kidney and bile increased quadratically (P<0.02) with increasing dietary concentrations of melamine. Compared with controls, melamine concentrations in liver and kidney were higher (P<0.001) in birds fed all levels of melamine, whereas melamine concentrations in breast muscle and bile were only higher (P<0.001) in birds fed≥1.0% melamine. Serum albumin, total protein, globulin, and calcium increased quadratically (P<0.02) in birds as dietary melamine increased, whereas serum aspartate transaminase and gamma gluatamyltransferase increased linearly (P<0.01) with increasing levels of melamine in the diet. Renal histopathology revealed nonpolarizable melamine crystals in the collecting tubules and ducts of birds fed≥1.5% melamine. In summary, dietary melamine was toxic to broilers at concentrations≥1.0%.

Efficacy of turmeric (Curcuma longa), containing a known level of curcumin, and a hydrated sodium calcium aluminosilicate to ameliorate the adverse effects of aflatoxin in broiler chicks.

A 3-wk feeding study was conducted to evaluate the efficacy of turmeric (Curcuma longa) powder (TMP), containing a known level of curcumin, and a hydrated sodium calcium aluminosilicate (HSCAS; Improved Milbond-TX, IMTX, an adsorbent, Milwhite Inc., Houston, TX) to ameliorate the adverse effects of aflatoxin B(1) (AFB(1)) in broiler chicks. Four pen replicates of 5 chicks each were assigned to each of 7 dietary treatments, which included the basal diet not containing TMP, HSCAS, or AFB(1) (control); basal diet supplemented with 0.5% food grade TMP that contained 1.48% total curcuminoids (74 mg/kg); basal diet supplemented with 0.5% HSCAS; basal diet supplemented with 1.0 mg/kg AFB(1); basal diet supplemented with 0.5% TMP and 1.0 mg/kg AFB(1); basal diet supplemented with 0.5% HSCAS and 1.0 mg/kgAFB(1); and basal diet supplemented with 0.5% TMP, 0.5% HSCAS, and 1.0 mg/kg AFB(1). The addition of TMP to the AFB(1) diet significantly (P < 0.05) improved the weight gain of chicks, and the addition of HSCAS to the AFB(1) diet significantly (P < 0.05) improved feed intake and weight gain, and reduced relative liver weight. The addition of TMP or HSCAS and TMP with HSCAS ameliorated the adverse effects of AFB(1) on some of the serum chemistry parameters (total protein, albumin, cholesterol, calcium). Further, decreased antioxidant functions in terms of level of peroxides, superoxide dismutase activity, and total antioxidant concentration in liver homogenate due to AFB1 were also alleviated by the inclusion of TMP, HSCAS, or both. The reduction in the severity of hepatic microscopic lesions due to supplementation of the AFB(1) diet with TMP and HSCAS demonstrated the protective action of the antioxidant and adsorbent used in the present study.

Pathologic changes in extrahepatic organs and agglutinin response to Salmonella Gallinarum infection in Japanese quail fed Fusarium verticillioides culture material containing known levels of fumonisin B1.

Three hundred 1-day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups of 150 each. One group was maintained on quail mash alone, whereas Fusarium verticillioides culture material (FCM) was added to quail mash in the second group from 5 days of age and supplied 150 mg FB1/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units [cfu]/ml) was given to groups CS and FS at 21 days of age. Three quail each, were necropsied on day 21 (0 day interval) from groups CX and FX, whereas at subsequent intervals, i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection (DPI), they were sacrificed from all four groups (CX, CS, FX, and FS) to study the agglutinin response to Salmonella Gallinarum and pathologic changes. The agglutinin titers to Salmonella Gallinarum in the combination group (FS) were generally lower when compared with those in group CS. A reduction in the size of spleen along with depletion of white pulp, thinning of cardiomyocytes, lymphoid cell depletion from bursal follicles, and renal tubular nephrosis were characteristic pathologic changes in group FX. In contrast, there was mild to severe enlargement of spleen accompanied by necrosis and reticuloendothelial cell hyperplasia, pericarditis, myocarditis, and focal interstitial nephritis in groups CS. Similar but more severe lesions were observed in the combination group (FS). In addition, the flabby texture of heart, hydropericardium, and ascites were mainly observed in group FS. It is concluded that continuous presence of fumonisins at 150 mg/kg diet increases the severity of Salmonella Gallinarum infection in young Japanese quail.

Individual and combined effects of Fusarium moniliforme culture material, containing known levels of fumonisin B1, and Salmonella gallinarum infection on liver of Japanese quail.

Three hundred day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups with 150 quail in each group. One group was maintained on quail mash alone, while Fusarium moniliforme culture material was added to quail mash in the second group from day 5 of age and was supplied at a rate of 150 ppm fumonisin B1 (FB1)/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units/ml) was given to groups CS and FS at 21 days of age. Three quail each were necropsied on day 21 (0 day interval) from groups CX and FX only. At subsequent intervals (i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection [DPI]), three quail were euthanatized from all four groups (CX, CS, FX, and FS). The gross and microscopic lesions were recorded in both mortality and euthanatized birds at the above intervals. The ultrastructural studies were done at 5 DPI. Mild to moderate hepatomegaly and pale discoloration of liver were observed in group FX, while congestion, hemorrhages, necrosis, and mild to severe hepatomegaly were the predominant gross lesions in both infected groups (CS and FS). The gross lesions in quail inoculated with Salmonella Gallinarum alone (group CS) generally developed slowly, appeared more widely scattered, and involved comparatively less surface area in contrast to the rapidly progressive and frequently confluent lesions in the combination group (FS), especially in the first 5 days of infection. Mild to marked hepatocellular swelling, multifocal hepatic necrosis, and hepatocellular and bile duct hyperplasia were the characteristic microscopic changes in the FX group. Microscopic lesions in quail of group CS comprised congestion, vacuolar changes, and focal necrosis in early stages, followed by granulomatous lesions at later intervals. Similar but more severe lesions were observed in the combination group (FS). Based on transmission electron microscopy, the maximum effect of FB1 toxicity was observed on mitochondria and endoplasmic reticulum. In general, the mitochondriae showed diverse form and structure, some of which appeared to lose their intact outer membrane, and the mitochondrial cristae were disoriented. The deformity in the cisternae structure of rough endoplasmic reticulum, with their rearrangement into round or tubular forms either bearing granular surface or leading to accumulation of smooth endoplasmic reticulum, was evident only in groups FX and FS. We conclude that the continuous presence of fumonisins in the diets of young quail might increase their susceptibility to or the severity of Salmonella Gallinarum infection.

Individual and combined effects of the Fusarium mycotoxins fumonisin B1 and moniliformin in broiler chicks.

The individual and combined effects of feeding fumonisin B1 (FB1; 0, 100, 200 mg FB1/kg) and moniliformin (M; 0, 100, 200 mg M/kg) were evaluated using a 3 x 3 factorial arrangement of treatments. Significant mortality (P < 0.05) occurred in chicks fed all diets containing 200 mg M/kg (50%-65%). Compared with controls and chicks fed FB1, both feed intake and body weight gain were decreased (P < 0.05) in chicks fed diets containing 100 mg M/kg. Chicks fed M had heavier heart weights (P < 0.05) than control chicks or chicks fed FB1. Compared with controls, chicks fed diets containing 200 mg M/kg or a combination of 200 mg FB1/kg and 100 mg M/kg had increased kidney and liver weights (P < 0.05). Significant FB1 by M interactions (P < 0.05) were observed for serum total protein and aspartate aminotransferase. Mild to moderate periportal extramedullary hematopoiesis and mild focal hepatic necrosis were observed in chicks fed FB1 alone. An increased incidence of large pleomorphic cardiomyocyte nuclei, loss of cardiomyocytes, and mild focal renal tubular mineralization were observed in chicks fed M alone. Both cardiac and renal lesions were observed in chicks fed combinations of FB1 and M. Data indicate FB1 and M, alone or in combination, can adversely affect chick performance and health at these dietary concentrations. The interactive effects of FB1 and M were not synergistic and were less than additive in nature. At the dietary concentrations studied, M is much more toxic to broilers than FB1.

Chronic effects of moniliformin in broiler and turkeys fed dietary treatments to market age.

Floor pen studies were conducted, with broilers from 1 to 7 wk of age and with turkeys from 1 to 14 wk of age, to evaluate the chronic effects of moniliformin (M). Fusarium fujikuroi (M-1214) culture material was added to typical corn-soybean basal diets to supply 0, 25, or 50 mg M/kg diet (broilers) or 0, 12.5, 25, 37.5, or 50 mg M/kg diet (turkeys). Compared with controls, chicks fed diets containing 50 mg M/kg consumed more feed, had lower body weight gain, were less efficient in converting feed to body weight gain, and had increased relative heart and proventriculus weights. Chicks fed the diet containing 50 mg M/kg also had significantly higher mortality and decreased mean corpuscular volumes compared with controls. Broilers fed 25 and 50 mg M/kg also had increased serum gamma glutamyltransferase activities. Feed intake, body weight gain, and feed conversion of turkeys fed dietary M were not affected. At 6 and 14 wk, turkeys fed 25, 37.5, or 50 mg M/kg diet had increased (P < 0.05) relative heart weights when compared with controls. At week 14, turkeys fed diets containing 37.5 or 50 mg M/kg also had increased (P < 0.05) relative liver weights compared with turkeys fed 0, 12.5, or 25 mg M/kg diet. Lesions, observed only in the hearts of broilers and turkeys fed 50 mg M/kg, were loss of cardiomyocyte cross striations, increased cardiomyocyte nuclear size, and an increased number of cardiomyocyte mitotic figures (turkeys only). Results indicate that > or = 37.5 mg M/kg is hepatoxic and > or = 25 mg M/kg is cardiotoxic to turkeys and 50 mg M/kg diet is toxic to broilers fed to market age.

Isolation from turkey breeder hens of a reassortant H1N2 influenza virus with swine, human, and avian lineage genes.

Type A influenza viruses can infect a wide range of birds and mammals, but influenza in a particular species is usually considered to be species specific. However, infection of turkeys with swine H1N1 viruses has been documented on several occasions. This report documents the isolation of an H1N2 influenza virus from a turkey breeder flock with a sudden drop in egg production. Sequence analysis of the virus showed that it was a complex reassortant virus with a mix of swine-, human-, and avian-origin influenza genes. A swine influenza virus with a similar gene complement was recently reported from pigs in Indiana. Isolation and identification of the virus required the use of nonconventional diagnostic procedures. The virus was isolated in embryonated chicken eggs by the yolk sac route of inoculation rather than by the typical chorioallantoic sac route. Interpretation of hemagglutination-inhibition test results required the use of turkey rather than chicken red blood cells, and identification of the neuraminidase subtype required the use of alternative reference sera in the neuraminidase-inhibition test. This report provides additional evidence that influenza viruses can cross species and cause a disease outbreak, and diagnosticians must be aware that the variability of influenza viruses can complicate the isolation and characterization of new isolates.

Chronic effects of fumonisin B1 in broilers and turkeys fed dietary treatments to market age.

Floor pen studies were conducted with 270 broiler chicks and 144 turkey poults, all 1 wk old, to evaluate the chronic effects of fumonisin B1 (FB1). A completely randomized design was used in both studies with six pen replicates of 15 chicks or eight pen replicates of six poults assigned to each of three dietary treatments from Weeks 1 to 7 (broilers) or to Week 14 (turkeys). Fusarium moniliforme (M-1325) culture material was added to a typical corn-soybean basal diet to supply 0, 25, or 50 mg FB1/kg diet. Feed intake, body weight gain, and feed conversion of chicks were not affected (P > 0.05) by FB1. Turkeys fed 50 mg FB1/kg had significantly (P < 0.05) lower feed intake than the controls. Compared with controls, chicks and turkeys fed FB1 diets had significantly higher liver sphinganine to sphingosine ratios (P < 0.05). Relative organ weights of chicks were not affected (P > 0.05) by FB1, other than those chicks fed 25 mg FB1/kg, which had lower (P < 0.05) relative proventriculus weights than the chicks fed 0 or 50 mg FB1/kg. Broilers fed 50 mg FB1/kg had decreased serum calcium and increased serum chloride when compared to broilers fed 0 or 25 mg FB1/kg. Hematology was not affected (P > 0.05) by dietary FB1. No lesions were present in any organ examined microscopically. Results indicate that 50 mg FB1/kg diet is detrimental to turkeys but is not toxic to broilers fed to market age.

Acute pulmonary Sarcocystis falcatula-like infection in three Victoria crowned pigeons (Goura victoria) housed indoors.

Three free-roaming Victoria crowned pigeons (Goura victoria) housed in a completely enclosed tropical exhibit were found dead without antemortem signs of illness. The birds died within 9 days of each other. Gross necropsy revealed moderate pulmonary edema in all three birds. Histopathologic examination revealed pulmonary edema and pulmonary protozoal merozoites compatible with Sarcocystis spp., Toxoplasma gondii, or Neospora spp. infection. Immunohistochemical staining for T. gondii and Neospora spp. were negative. Immunohistochemical staining identified a Sarcocystis falcatula-like parasite in all three birds. It is suspected that new exhibit soil contaminated with feces from the Virginia opossum (Didelphis virginiana) was the source of the infective sporocysts.

Blood plasma chemistries from wild mourning doves held in captivity.

Despite the extensive amount of research conducted on mourning doves (Zenaida macroura), no biochemical reference values exist for this species. Our objective, therefore, was to establish base line clinical chemistry reference values for mourning doves to assist with establishing clinical diagnoses. Wild mourning doves were captured 19 March 1996 to 8 August 1996, and 6 February 1998 to 12 May 1998; blood samples were collected from 382 mourning doves. Plasma biochemical values were established for glucose, sodium, potassium, chloride, enzymatic CO2, albumin, total protein, globulin, calcium, phosphorus, cholesterol, magnesium, aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), and uric acid. These reference values are invaluable for determining diagnosis of diseases of the gastrointestinal, hepatic, renal, cardiovascular, musculoskeletal, and endocrine systems.

Polytetrafluoroethylene gas intoxication in broiler chickens.

A poultry research facility that housed 2400 Peterson x Hubbard cross broilers (48 pens of 50 chicks each) experienced 4% mortality within 24 hr of chick placement. Mortality started within 4 hr of placement, and within 72 hr, cumulative mortality had reached 52%. Mild dyspnea was the only clinical sign noted in some chicks prior to death. The primary gross lesion noted in the chicks submitted was moderate to severe pulmonary congestion. The lungs of four of these chicks sank in formalin, and blood-tinged fluid was noted in the mouth and nares of two chicks. The microscopic lesions noted in the affected chicks were moderate to severe pulmonary edema and congestion. The diagnosis indicated to the submitter was that pulmonary edema caused by exposure to an unidentified noxious gas caused the death of the chicks. The poultry house environment was tested for sulfur dioxide, oxides of nitrogen, carbon monoxide, carbon dioxide, and volatile organic compounds (as produced by combustion engines); all tests were negative for significant levels of these compounds. A second broiler flock was placed in the same facility and the mortality at 6 wk was 11%, which was greater than the 2.5%-4.7% mortality seen in the previous four flocks on the farm. Further investigation revealed that the only change in management practice in this facility prior to the onset of the severe mortality problem was the replacement of 48 heat lamp bulbs (one for each pen). The new heat lamp bulbs were polytetrafluoroethylene (PTFE) coated. PTFE gas intoxication has been reported in several exotic avian species, but this intoxication has not been previously reported in a poultry flock.

The individual and combined effects of fumonisin B1 and moniliformin on performance and selected immune parameters in turkey poults.

Effects of feeding diets containing fumonisin B1 (FB1) and moniliformin (M), singly or in combination, on performance and immune response were evaluated in poults. Day-old poults were randomly assigned to one of four dietary treatments with four replicates of four poults each. Dietary treatments were 1) control; 2) 200 mg FB1, 0 mg M/kg diet; 3) 0 mg FB1, 100 mg M/kg diet; and 4) 200 mg FB1, 100 mg M/kg diet. In Experiment 1, poults were injected with 0.25 mL Newcastle disease virus (NDV) vaccine on Weeks 2 and 3 of the experiment, and anti-NDV antibody titers were measured 7 d after each injection. Compared with controls, poults fed FB1 had significantly lower (P < 0.05) secondary antibody response. Poults fed M and the combination of FB1 and M had significantly lower (P < 0.05) primary and secondary antibody response. Lower relative thymus weights were observed in poults fed diets containing FB1 or M. Decreased relative bursa and spleen weights were observed in poults fed M. In Experiment 2, poults were placed on dietary treatments for 3 wk. On Day 21, 2 x 10(6) peripheral lymphocytes were incubated with mitogens. Poults fed diets containing FB1 had a significantly lower (P < 0.05) proliferative response to mitogens in comparison to controls. In Experiment 3, poults were placed on the diets for 3 wk and were injected with 4.4 x 10(7) E. coli/kg body weight on Day 21. Significantly higher (P < 0.05) numbers of E. coli colonies were observed in the blood and tissue homogenates of poults fed M. In all three experiments, feed intake and body weight gains were significantly lower (P < 0.05) in turkeys fed diets containing M. Data from the present study suggest that FB1 and M are immunosuppressive in poults and that M not only suppresses immune response but also performance. However, neither synergistic nor additive effects between FB1 and M were observed for any of the parameters measured.

Effects of moniliformin on performance and immune function of broiler chicks.

Three trials were conducted to evaluate the effect of moniliformin (M) on performance and immune function in chicks. Day-old chicks were randomly assigned to four dietary treatments (0, 50, 75, or 100 mg M/kg diet). In Trial 1, chicks were placed on treatments for 3 wk and were injected intravenously with 4.6 x 10(6) Escherichia coli on Day 21. Blood samples were collected at 60, 120, and 180 min after inoculation, and liver, spleen, and lung were collected at 180 min postinjection. Compared with control chicks, chicks fed 75 and 100 mg M/ kg diet had higher (P < 0.05) numbers of E. coli colonies in the circulation, liver, and spleen. In Trial 2, chicks were placed on diets for 4 wk and were injected with 0.5 mL Newcastle disease virus (NDV) vaccine intramuscularly on Weeks 2 and 3 of the experiment. The primary and secondary anti-NDV antibody titers were measured 7 d after each injection. Chicks fed 100 mg M/kg diet had lower (P < 0.05) secondary antibody titers than did control chicks. In Trial 3, lymphocyte proliferation in chicks exposed to M in vivo and in vitro was determined. Results of the in vivo study showed that cell proliferation in response to mitogens from control- and M-fed chicks did not differ (P > 0.05). For the in vitro study, lymphocyte proliferation decreased linearly (P < 0.01) with increased concentrations of M. In all three trials, chicks fed 100 mg M/kg diet had lower (P < 0.05) feed intake and weight gain than did control chicks. Data from the current study suggested that M decreased performance and immune response in chicks at the level of 75 mg/kg diet.

Effects of fumonisin B1 on selected immune responses in broiler chicks.

Three experiments were conducted to evaluate immune responses in chicks fed fumonisin B1 (FB1). Day-old male chicks were randomly allotted to dietary treatments: 0, 50, 100, or 200 mg FB1/kg diet. In Experiment 1, chicks were fed diets for 3 wk and were injected intravenously with 4.6x10(6) Escherichia coli on Day 21. Blood samples were collected at 60, 120, and 180 min postinjection, and liver, spleen, and lung were collected after 180 min. Chicks fed 200 mg FB1/kg diet had significantly higher numbers of bacterial colonies in blood, spleen, and liver (P<0.05) than control chicks. In Experiment 2, chicks were placed on the diets for 4 wk and were injected with 0.5 mL inactivated Newcastle Disease virus vaccine on Weeks 2 and 3 of the experiment, and primary and secondary antibody titers were measured 7 d after each injection. The secondary antibody response in chicks fed 200 mg FB1/kg diet was significantly lower (P<0.05) than that of control chicks. In Experiment 3, lymphocyte proliferation in chicks exposed to FB1 in vivo or in vitro was determined. Results of the in vivo study showed that cell proliferation in response to mitogens was lower (P<0.05) in chicks fed 200 mg FB1/kg diet than in control chicks. For the in vitro study, cell proliferation was lower (P<0.05) when cells were exposed to > or = 2.5 microg FB1/mL. Data of the current study suggested that FB1 is immunosuppressive in chicks when present in the ration at 200 mg FB1/kg diet.

The individual and combined effects of feeding moniliformin, supplied by Fusarium fujikuroi culture material, and deoxynivalenol in young turkey poults.

The effects of feeding diets containing either 20 mg deoxynivalenol (DON)/kg, 100 mg moniliformin (M)/kg, or a combination of DON and M (20 mg/kg DON and 100 mg M/kg) were evaluated in growing turkey poults, from 1 to 21 d of age. Feed intake and BW gains were decreased (P < 0.05) by dietary treatments containing M. Feed conversion was not affected by any of the dietary treatments, and no interactive effects on performance were evident between M and DON. Absolute weights of hearts and kidneys were increased (P < 0.05) in poults fed diets containing M. Mean cell volume was decreased by the M and DON-M treatments; however, the decrease was much smaller in poults fed the combination DON-M treatment resulting in a significant (P < 0.05) DON by M interaction. Mean cell hemoglobin and mean cell hemoglobin concentrations were not affected by any of the dietary treatments. No histological lesions were seen in control poults or poults fed DON alone. Lesions associated with dietary treatments were only observed in the heart and kidney. Poults fed diets containing M alone or the DON-M combination exhibited an increased incidence of variable sized cardiomyocyte nuclei, with numerous large giant nuclei, and a generalized loss of cardiomyocyte cross striations. Isolated renal tubules in sections of kidney were noted to have mild diffuse mineralization in poults fed M and the combination DON-M treatments. None of the response variables measured were affected by DON alone. No toxic synergy was observed when these toxins were fed simultaneously to turkey poults for 21 d.

Efficacy of a hydrated sodium calcium aluminosilicate to ameliorate the toxic effects of aflatoxin in broiler chicks.

In vitro and in vivo studies were conducted to evaluate the efficacy of a hydrated sodium calcium aluminosilicate (Improved Milbond-TX, IMTX) to alleviate the toxic effects of aflatoxin (AF) B1 in chicks. In vitro results indicated that IMTX was able to bind 100% of AFB1 at pH 3 to 9. In the in vivo study, five pen replicates of six chicks were assigned to each of four dietary treatments, which included: 1) basal diet containing neither IMTX nor AFB1 (control); 2) basal diet supplemented with 1% IMTX; 3) basal diet supplemented with 4 mg AFB1/kg diet; and 4) basal diet supplemented with 1% IMTX and 4 mg AFB1/kg diet. The addition of IMTX to chick diets at a level of 1% did not negatively affect chick performance, organ weights, or serum chemistry, or cause pathological changes. Improved Milbond-TX completely prevented the reduced performance, changes in organ weights, serum chemistry changes, and gross pathology observed in chicks fed AFB1. The IMTX dramatically reduced the incidence and severity of the hepatic histopathology changes associated with aflatoxicosis and completely prevented the renal lesions of aflatoxicosis. These results indicated that IMTX was effective in preventing the toxic effects of AF that may be present in poultry rations at levels up to 4 mg/kg feed.

Effects of biogenic amines in broiler chickens.

Biogenic amines in spoiled animal by-product feeds have been implicated in causing poor performance and intestinal lesions in broilers. This study was designed to determine if biogenic amines, at the concentrations found in animal by-product meals, would reduce performance in broilers or cause lesions. Twelve treatments were used in a 2 x 6 factorial arrangement with the main effects being either a corn-soybean meal diet or a corn-soybean meal diet with 10% animal by-products added and either no amines added or added levels of phenylethylamine (4.8 mg/kg), putrescine (49 mg/kg), cadaverine (107 mg/kg), histamine (131 mg/kg), or a combination of all these amines. Levels of biogenic amines used in this study simulated those found in areas with reported problems attributed to biogenic amines. Broilers were monitored for performance, gross lesions, and histologic evidence of lesions at 2, 4, and 6 wk. No consistent effects were observed on performance, and by the conclusion of the trial, no statistical differences were noted in the performance of any of the treatments. No gross lesions were observed on a consistent basis in any of the treatments. Histopathology was likewise unremarkable. On the basis of this study, it would appear that these four biogenic amines, at levels detected in the United States, do not pose a serious health concern for the broiler industry.

Unusual gangliosidosis in emu (Dromaius novaehollandiae).

A previous study has demonstrated an unusual gangliosidosis in emu that is characterized by the accumulation of gangliosides in the brain tissues with GM3 and GM1 predominating. To provide insight into this unique disorder of emu gangliosidosis, the current study focused on analysis of neutral glycosphingolipids and gangliosides from brain and liver tissues of affected birds and healthy controls. We found not only that the total lipid-bound sialic acid content was increased three- and fourfold in the affected brain and liver, respectively, but also that the ganglioside pattern was rather complex as compared with the control. The absolute ganglioside sialic acid content was significantly increased in the diseased tissues, with the highest elevation levels of GM3 (14-fold) and GM1 (ninefold) in the affected brain. Relative increases in content of these monosialogangliosides were also significant. GM2 was only detected in the affected brain, but not in normal controls. The neutral glycosphingolipid fraction showed accumulation of many oligosylceramides, with six- and 5.5-fold increases in lactosylceramide levels for brain and liver, respectively. The level of myelin-associated galactosylceramide (GalCer) in the brain was decreased to only 41% of that in the healthy control, whereas no difference was found in liver tissues from both groups. Besides GalCer, the brain content of sulfatide (cerebroside-sulfate esters), another myelin-associated glycolipid, decreased to only 16% of the control. The loss of myelin-associated GalCer and sulfatide strongly suggests demyelination in the affected emu brain. Our overall data are consistent with the presence of a unique form of sphingolipidosis in the affected emus, perhaps with secondary demyelination, and suggest a metabolic disorder related to total sphingolipid activator deficiency.