Effects of Feeding Nivalenol-Contaminated Diets to Male Broiler Chickens

Abstract

In two feeding trials the effect of nivalenol (NIV) on male broiler chickens was studied. A commercial starter diet was provided for ad libitum consumption throughout the whole experiment. The NIV was added to the feed when the birds were 7 d old. Growth and feed consumption were thereafter registered every 5th d during 20 d. In the first trial birds were offered feed containing 0, .5, 2.5, or 5 ppm NIV. The only variable that significantly differed from the control was the concentration of uric acid in plasma, which was increased by 94 and 66%, respectively, in treatment groups 2.5 and 5 ppm. In the second trial, NIV-concentrations of 0, 3, 6, and 12 ppm were used. The weight gain for the 20-d period was decreased by 11% with 6 and 12 ppm. During this period these birds showed a decrease of about 6% in feed consumption and feed conversion efficiency. Gizzard erosions were found in 33% of the birds fed 12 ppm NIV and in 8% of those fed 3 or 6 ppm. No such erosions were found in the control birds. Relatively, the liver weights in the 12 ppm group were reduced more than total body weights. No effects on relative organ weights were found when bursa, spleen, and gizzard were compared to control. In the blood, no change compared to control was found in hematocrit or in the plasma concentration of glucose, calcium, cholesterol, triglycerides, and uric acid, or in the plasma activity of aspartate amino transferase, alanine amino transferase, or gamma glutamyl transpeptidase.

Effect of subacute oral doses of nivalenol on immune and metabolic defence systems in mice

“…Certain parameters like sodium or chlorine appeared to be insensitive to nivalenol as previously demonstrated in the chicken [7]. Alkaline phosphatase activity was increased whereas plasma urea, glucose, triglycerides and cholesterol levels were decreased in the group of mice receiving the highest dose of NIV.…”

Association between gizzard lesions and increased caecalClostridium perfringenscounts in broiler chickens

“…GEU has also been found recently in commercial broiler flocks in Norway (unpublished data). Previous studies have linked GEU occurrence with several nutritional and infectious factors (Poupoulis & Jensen, 1976;Okazaki et al 1983;Fossum et al ., 1988;Hedman et al ., 1995;Kaya et al ., 2002;Hetland et al ., 2003;Ono et al ., 2003a;). C. perfringens has been isolated from chickens with gizzard lesions, but the aetiological role of C. perfringens in this condition is uncertain.…”

“…A condition designated ''gizzard erosions'' and/or ''gizzard ulceration'' (GEU) has been reported in commercial broiler chickens in connection with avian adenovirus infection (Ono et al ., 2001(Ono et al ., , 2003a, mycotoxin-contaminated feed (Hedman et al ., 1995;Hoerr, 2003), vitamin B 6 deficiency (Daghir & Haddad, 1981), suboptimal levels of vitamin E (Janssen & Germs, 1973), inadequate levels of sulphur-containing dietary amino acids (Miller et al ., 1975), high levels of dietary copper (Poupoulis & Jensen, 1976), pelleted feed (Ross, 1979), as well as inclusion of certain fish meals in the diets and the consequent presence of histamine and gizzerosine (Harry & Tucker, 1976;Okazaki et al ., 1983;Sugahara et al , 1988;Sharma & Pandey, 1990;Tisljar et al , 2002). The koilin layer of gizzards from affected birds is fissured, thickened, spongy and discoloured (Fossum et al ., 1988).…”

Enzootic outbreak of necrotic gastritis associated withClostridiumperfringensin broiler chickens

“…A condition termed ''gastric erosions'' and/or ''gastric ulcerations'' has been reported in commercial broiler chickens in association with avian adenovirus infection (Ono et al, 2001(Ono et al, , 2003a, mycotoxin-contaminated feed (Hedmann et al, 1995;Hoerr, 2003), vitamin B 6 deficiency (Daghir & Haddad, 1981), suboptimal vitamin E concentrations (Janssen & Germs, 1973), inadequate levels of sulphur-containing amino acids (Miller et al, 1975), high dietary copper concentrations (Poupolis & Jencen, 1976), pelleted feed (Ross, 1979), as well as with the inclusion of some fish meals in feeds with subsequent release of histamine and gizzerosine (Harry & Tucker, 1976;Okazaki et al, 1983;Sugahara et al, 1988;Sharma & Pandey, 1980;Tisljar et al, 2002). In these instances, the cuticle of the gizzard in affected birds appeared fissured, thickened and with altered colour (Fossum et al, 1988).…”