In the present study, 256 7-wk-old Japanese quail were randomly distributed into four experimental groups (64 birds per group) and given rations containing 0 (controls), 25, 50, or 100 (g aflatoxin B, (AFB1)/kg feed for 168 d. Each treatment consisted of four replicates of 16 quail. Egg production and individual egg weight were checked daily. Feed consumption and feed use were determined weekly. Eggs laid in the last day of each 28-d laying period were collected and subjected to individual analysis for specific gravity, Haugh units, shell thickness and percentage eggshell. Results showed that average egg production, feed use, and body weights were not affected (P > 0.05) by AFB1. However, feed consumption was lower (P < 0.05) for groups fed 50 or 100 microg AFB1/kg. Egg weight was significantly lower (P < 0.05) only for groups exposed to 50 and 100 microg AFB1/kg. Average egg specific gravity, Haugh units, and shell thickness were not affected (P > 0.05) by AFB1. Percentage eggshell was higher (P < 0.05) in the group fed the ration containing 100 microg AFB1/kg. Treatment associated lesions were observed only in the liver. Hepatic cell vacuolation with fatty infiltration was observed in all liver samples of quail fed AFB1-contaminated rations. Bile duct proliferation and trabecular disorder were found only in livers of quail on the 100-microg AFB1/kg treatment. Results indicated that chronic exposure to AFB1 at levels above 50 microg/kg could adversely affect quail performance, emphasizing the importance of controlling aflatoxin contamination in quail rations.

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In the present study, 288 8-wk-old Japanese quail were randomly distributed into 6 experimental groups (48 birds per group) and fed the following diets for 140 d: 1) 0 (control); 2) 10 mg of fumonisin B1 (FB1); 3) 50 microg of aflatoxin B1 (AFB1); 4) 50 microg of AFB1 + 10 mg of FB1; 5) 200 microg of AFB1; and 6) 200 microg of AFB1 + 10 mg of FB1/kg of feed. Each treatment consisted of 4 replicates of 12 quail. Egg production and individual egg weight were checked daily. Feed intake and feed conversion were determined weekly. Results showed that by the end of the fifth cycle, average egg weight was lower (P < 0.05) in groups fed 10 mg of FB1/kg, 50 microg of AFB1/kg, 200 microg of AFB1/kg, and 10 mg of FB1 + 50 microg of AFB1/kg of feed. Egg production decreased (P < 0.05) in birds fed 10 mg of FB1/kg by the third, fourth, and fifth cycles. Feed intake was lower (P < 0.05) in birds fed 10 mg of FB1/kg by the fourth and fifth cycles, and in birds fed 50 and 200 microg of AFB1/kg in the fifth cycle. Birds fed 10 mg of FB1 + 50 microg of AFB1/kg consumed less feed (P < 0.05) in the first, second, and fifth cycles. Results indicated that prolonged administration of FB1 and AFB1, singly or in combination at the levels evaluated, may cause economic losses to quail egg producers.

The aim was to evaluate the excretion of residues of aflatoxin B(1) (AFB(1)), aflatoxin M(1) (AFM(1)), aflatoxin B(2a) (AFB(2a)) and aflatoxicol (AFL) in eggs of laying Japanese quail fed rations with low levels of aflatoxin B(1) for 90 days. The quail were randomly assigned into four experimental groups and given prepared rations containing either 0 (controls), 25, 50 or 100 microg AFB(1) kg(-1) feed. Thirty-two eggs per treatment were collected on days 1-7, 10, 20, 30, 60 and 90 of the aflatoxin treatment period, and submitted to aflatoxin analysis by high-performance liquid chromatography. Average egg production and feed consumption were not affected ( p > 0.05) by AFB(1). Egg weight was significantly lower ( p<0.05) only for groups exposed to 100 microg AFB(1) kg(-1). Residues of aflatoxins were detected in eggs at levels that ranged from 0.01 to 0.08 microg kg(-1) (AFB(1)), 0.03-0.37 microg kg(-1) (AFM(1)), 0.01-1.03 microg kg(-1)(AFB(2a)) and 0.01-0.03 microg kg(-1) (AFL). Results indicate that the excretion of aflatoxin residues in quail eggs might occur at relatively low concentrations under conditions of long-term exposure of quail to low levels of AFB(1).

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