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D R Ledoux

Publications and source records attributed to D R Ledoux.

42 records · Page 3Linked to original sources

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.

Animal Feed↗

Effects on turkey poults of feeding Fusarium moniliforme M-1325 culture material grown under different environmental conditions.

The effects of feeding Fusarium moniliforme M-1325 culture material (CM), grown under different environmental conditions, were studied in turkey poults. Poults were fed a control diet or diets containing four levels of FB1 (75, 150, 225, or 300 mg/kg) prepared from F. moniliforme M-1325 cultures that produced 7800 (CM1) or 4000 mg FB1/kg (CM2). F. moniliforme M-1325 CM that produced a low concentration of FB1 (350 mg FB1/kg) was also used to prepare an additional diet containing 75 mg FB1/kg (CM3). Dose-dependent decreases in feed intake and body-weight gains and dose-dependent increases in liver weights and serum sphinganine (SA) to sphingosine (SO) ratios were observed in poults fed CM1 or CM2. Poults fed CM3 consumed more feed and had lower body-weight gains than controls or poults fed CM1 or CM2 (at 75 mg FB1/kg). Poults fed CM3 also had increased liver weights and SA:SO ratios compared with control poults. Generalized hepatocellular hyperplasia was observed in all FB1 treatment groups. Biliary hyperplasia was evident in turkeys fed 150 to 300 mg FB1/kg. Results indicate that at equivalent dietary FB1 levels, F. moniliforme cultures producing different concentrations of FB1 differ in their effects on turkey poults.

Animal Feed↗

The chronic effects of Fusarium moniliforme culture material, containing known levels of fumonisin B1, in turkeys.

Fourteen 1-day-old male turkeys were randomly assigned to two adjacent floor pens and fed balanced rations containing 0 and 75 mg fumonisin B1 (FB1)/kg for 18 weeks. Inclusion of FB1 in the ration caused decreased body weight gain on weeks 4, 10, and 12 during the trial. Turkeys fed 75 mg FB1/kg had significantly heavier livers after treatment for 18 weeks. Chronic FB1 exposure resulted in an increased total white blood cell count, absolute heterophil count, absolute lymphocyte count, and heterophil-to-lymphocyte ratio. No mortality was noted in turkeys in either treatment group. Turkeys are relatively resistant to chronic FB1 exposure.

Animals↗

Effects of Fusarium moniliforme culture material containing known levels of fumonisin B1 in ducklings.

Fusarium moniliforme culture material containing fumonisin B1 (FB1) was fed to white Pekin ducklings from 1 to 21 days of age. Four dietary treatments were prepared with 0, 100, 200, and 400 mg FB1/kg ration. Ducklings fed rations containing FB1 had a dose-dependent decrease in feed intake and weight gain. Increasing levels of FB1 in the ration were associated with increasing absolute organ weights of liver, heart, kidney, pancreas, and proventriculus. Liver sphinganine to sphingosine ratios increased significantly in ducklings fed FB1. Two of eight ducklings fed a ration containing 400 mg FB1/kg died prior to the termination of the experiment. Mild to moderate hepatocellular hyperplasia was evident in all ducklings fed FB1. Mild to moderate biliary hyperplasia was also noted in the liver sections of ducklings fed 400 mg FB1/kg in the ration. Ducklings, like other poultry, are relatively resistant to the toxic effects of FB1.

Animal Feed↗

The individual and combined effects of the Fusarium mycotoxins moniliformin and fumonisin B1 in turkeys.

Fumonisin B1 (FB1) and moniliformin (M) were supplied by Fusarium moniliforme M-1325 and Fusarium fujikuroi M-1214 culture material, respectively. Turkeys were fed a control ration, or rations containing 200 mg FB1/kg, 100 mg M/kg, or a combination of both 200 mg FB1/kg and 100 mg M/kg feed from 1 to 21 days of age. These rations contained 0, 3.8, 1.0, and 4.8% culture material, respectively. In comparison to controls, turkeys fed FB1 had increased relative liver weights. Both aspartate aminotransferase and lactate dehydrogenase were increased in poults fed FB1. Turkeys fed M had decreased feed intake and body weight gains and increased relative heart weights in comparison to controls. Poults fed FB1 had moderate diffuse hepatocellular hyperplasia and poults fed moniliformin had a loss of cardiomyocyte cross striations. Turkeys fed the ration containing both M and FB1 had all the above changes; however, no additive or synergistic effects were evident for any single parameter measured. No treatment-related morbidity or mortality was observed in the study.

Animal Feed↗

Heritability and biochemistry of gangliosidosis in emus (Dromaius novaehollandiae).

The progeny of two emu breeder pairs, which had a history of producing offspring with gangliosidosis, were monitored for 15 mo. DNA fingerprinting revealed that individuals in each breeder pair were not related to each other. One breeder pair had 13 progeny that reached or exceeded the age of 1 mo, and six of these progeny developed gangliosidosis. The mean age at which these affected emus were euthanatized, with distinct neurologic disease, or died was 5.7 mo. The second emu pair had 13 progeny, seven of which developed gangliosidosis, with a mean age of euthanasia/death of 4.6 mo. Affected emus died or were euthanatized from 2 to 8 mo of age. The primary clinical sign in the affected emus was mild to severe ataxia. Severe hemorrhage into the body cavity or the muscles of the thigh was noted in 8 of 13 of the affected emus. Brain ganglioside levels were evaluated in six of the affected emus and six controls. Significant increases (P < 0.05) in gangliosides GM1 and GM3 were noted, with 2.3- and 4.9-fold increases in these two gangliosides, respectively, in affected emus. Furthermore, the diseased emu brains contained ganglioside GM2, whereas this monosialoganglioside was undetectable in the brains of normal controls. Total mean brain ganglioside sialic acid in affected emus was increased 3.3-fold in comparison with controls. Serum chemistries revealed elevated cholesterol and decreased uric acid levels in affected emus. Gangliosidosis in emus is an inherited disease process that, in the current study, caused 50% mortality in the progeny of two emu breeder pairs. The elimination of this lethal gene from emu breeder stock is essential for the long-term economic viability of the United States emu industry.

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