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In the present study, the potential for carry-over of deoxynivalenol (DON) into eggs and DON residues in plasma and bile of laying hens of different genetic backgrounds after long-term feeding trial was investigated. A total of 80, 23-week-old laying hens were assigned to a feeding trial with two diets, a control diet and a Fusarium toxin-contaminated diet (FUS) (0.4 and 9.9 mg DON kg(-1), respectively). In the 60th week of hen's life, 10 eggs from each group were collected. In the 70th week of hen's life, all hens were slaughtered and samples of blood and bile were collected. The samples were analysed by liquid chromatography tandem mass spectrometry (LC-MS/MS) for DON and de-epoxy-DON. DON was only detected in samples of hens which fed the FUS diet while none of the samples analysed had detectable levels of de-epoxy-DON. In plasma and bile samples, DON levels ranged from 0.2 to 0.6 ng ml(-1) and from 1.8 to 4.1 ng ml(-1), respectively. DON levels in egg yolk and albumen ranged between 0.0-0.46 ng g(-1) and 0.0-0.35 ng g(-1), respectively, corresponding to carry-over rates of DON into eggs from 0.0 to 0.000016. Moreover, no differences in DON levels or carry-over rates were noticed between the two tested breeds. These results show that very low levels of DON were transferred into eggs and indicate that although eggs could contribute to human exposure to DON, the levels are very low and insignificant.

Although acute mycotoxicoses are rare in poultry production, chronic exposure to low levels of mycotoxins is responsible for reduced productivity and increased susceptibility to infectious diseases. Deoxynivalenol (DON) is known to modulate immune function, but only a few studies have investigated the effect of DON on the vaccinal immune response. In addition, the effects of Mycofix select (Biomin GmbH, Herzogenburg, Austria) supplementation to DON-contaminated broiler diets have not yet been demonstrated. Therefore, an experiment with 1-d-old male broilers (Ross 308) was carried out to examine the effects of feeding DON-contaminated low-protein grower diets on performance, serum biochemical parameters, lymphoid organ weight, and antibody titers to infectious bronchitis vaccination in serum and to evaluate the effects of Mycofix select dietary supplementation in either the presence or absence of DON in broilers. In total, thirty-two 1-d-old broiler chicks were randomly assigned to 1 of the 4 dietary treatments for 5 wk. The dietary treatments were 1) control; 2) artificially contaminated diets with 10 mg of DON/kg of diet; 3) DON-contaminated diets supplemented with Mycofix select; and 4) control diet supplemented with Mycofix select. Feeding of contaminated diets decreased (P = 0.000) the feed intake, BW (P = 0.001), BW gain (P = 0.044), and feed efficiency during the grower phase. Deoxynivalenol affected the blood biochemistry, whereas plasma total protein and uric acid concentrations in birds fed contaminated grains were decreased compared with those of the controls. Moreover, in birds fed contaminated feeds, there was a tendency to reduce triglycerides in the plasma (P = 0.090), suggesting that DON in the diets affected protein and lipid metabolism in broiler chickens. The feeding of contaminated diets altered the immune response in broilers by reducing the total lymphocyte count. Similarly, the antibody response against infectious bronchitis vaccination antigens was decreased (P = 0.003) after feeding contaminated diets, compared with the controls. Moreover, contamination of the broiler diet with DON increased the heteropil:lymphocyte ratio (stress index), suggesting that DON elevated the physiological stress responses of broilers. However, feeding of DON-containing diets did not alter the other plasma constituents, including activities of enzymes. Mycofix select addition to the DON-contaminated feed led to normal immunological and physiological functions in broilers that were comparable with those of the control group, indicating that the addition of the additive to the DON-contaminated feed of the broilers effectively alleviated the alterations caused by DON. It was concluded that broiler performance and some blood and immunological parameters were adversely affected by feeding diets contaminated with the Fusarium mycotoxin DON. However, the dietary Mycofix select supplementation as a detoxifying agent was successful in overcoming the mycotoxin-related effects.

A meta-analysis was carried out to study the association of mycotoxins with performance, productive indices, and organ weights in broilers. Ninety-eight papers published between 1980 and 2009 were used, totaling 1,401 diets and 37,371 animals. Meta-analysis followed 3 sequential analyses: graphical, correlation, and variance-covariance. The mycotoxin presence in diets reduced (P < 0.05) feed intake by 12% and weight gain by 14% compared with control group. Ochratoxins and aflatoxins were the mycotoxins with the greatest effect on feed intake and bird growth, reducing (P < 0.05) feed ingestion by 17 and 11%, respectively, and weight gain by 20 and 11%, respectively. The mycotoxin concentration in diets and the animal age at challenge were the variables that more improved the coefficient of determination for equations to estimate mycotoxin effect on weight gain. The mycotoxin effect on growth proved to be greater in young poultry. The residual analysis revealed that 65% of the variation in weight gain was explained by feed intake. The variation in weight gain of challenged broilers in relation to nonchallenged broilers was also influenced by ingestion of nutrients such as protein and methionine. Mortality was 8.8 and 2.8 times greater (P < 0.05) in groups that received diets with deoxynivalenol and aflatoxins, respectively. Mycotoxins also increased (P < 0.05) the relative weight of liver by 15%, of kidneys by 11%, of lungs by 9%, and of gizzard by 3%. Mycotoxins influenced broiler performance, productive indices, and organ weights. However, the magnitude of the effects varied with type and concentration of mycotoxin, animal age, and nutritional factors.

A study was conducted to investigate the effects of feeding grains naturally contaminated with Fusarium mycotoxins on performance and metabolism of broiler breeders. Forty-two 26-wk-old broiler breeder hens and nine 26-wk-old roosters were fed the following diets: (1) control, (2) contaminated grains, and (3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA) for 12 wk. The major contaminant was deoxynivalenol (12.6 mg/kg of feed), with lesser amounts of zearalenone and 15-acetyl-deoxynivalenol. Feed consumption and BW were not affected by diet. The feeding of contaminated grains did not significantly affect egg production. Decreased eggshell thickness was seen, however, at the end of wk 4, and dietary supplementation with GMA prevented this effect. There was no effect of diet on other egg parameters measured. There was a significant increase in early (1 to 7 d) embryonic mortality in eggs from birds fed contaminated grains at wk 4, but mid- (8 to 14 d) and late- (15 to 21 d) embryonic mortalities were not affected by diet. There were no differences in newly hatched chick weights or viability. The ratio of chick weight to egg weight was not affected by the feeding of contaminated grains. Weight gains of chicks fed a standard broiler starter diet at 7, 14, and 21 d of age were not significantly affected by previous dietary treatments for the dam. It was found that rooster semen volume and sperm concentration, viability, and motility were not affected by the feeding of contaminated diets. There was no effect of diet on the relative weights of liver, spleen, kidney, and testes. The feeding of contaminated grains decreased antibody titers against infectious bronchitis virus at the end of wk 12, and this was prevented by dietary supplementation with GMA. There was no effect of the diet on serum antibody titers against Newcastle disease virus. It was concluded that the feeding of blends of grains contaminated with Fusarium mycotoxins could affect performance and immunity in broiler breeder hens.

Feeding grains naturally contaminated with Fusarium mycotoxins has been shown to alter metabolism and performance of laying hens. The objectives of the current experiment were to examine the effects of feeding grains naturally contaminated with Fusarium mycotoxins on hematology and immunological indices and functions of laying hens and the possible protective effect of feeding a polymeric glucomannan mycotoxin adsorbent (GMA). One hundred forty-four laying hens were fed for 12 wk with diets formulated with (1) uncontaminated grains, (2) contaminated grains, or (3) contaminated grains + 0.2% GMA. Fusarium mycotoxins such as deoxynivalenol (DON, 12 mg/kg), 15-acetyl-DON (0.5 mg/kg), and zearalenone (0.6 mg/kg) were identified in the contaminated diets arising from contaminated grains grown in Ontario, Canada. The concentrations of DON arising from naturally contaminated grains in this study were similar to purified mycotoxin fed to experimental mice. The chronic feeding of Fusarium mycotoxins induced small decreases in hematocrit values, total numbers of white blood cells, lymphocytes including both CD4+ and CD8+ T lymphocytes and B lymphocytes, and biliary IgA concentration. Supplementation of diets containing feedborne mycotoxins with GMA prevented the reduction in total number of B lymphocytes in the peripheral blood and the reduction in biliary IgA concentration. In addition, the delayed-type hypersensitivity response to dinitrochlorobenzene was increased by feed-borne mycotoxins, whereas IgG and IgM antibody titers to sheep red blood cells were not affected by diet. We concluded that chronic consumption of grains naturally contaminated with Fusarium mycotoxins at levels likely to be encountered in practice were not systemically immunosuppressive or hematotoxic; however, mucosal immunocompetence needs to be explored further.

Experiments were conducted to evaluate the effects of feeding grains naturally contaminated with a combination of Fusarium mycotoxins on hepatic fractional protein synthesis rates (FSR) of laying hens. Thirty-six 32-wk-old laying hens were fed diets formulated with 1) uncontaminated grains, 2) contaminated grains, or 3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent for a period of 4 wk. Hepatic FSR were measured in vivo by the flooding-dose method. The feeding of contaminated grains decreased hepatic FSR in laying hens compared with controls after 4 wk. The hepatic FSR of birds fed contaminated grains and contaminated grains + glucomannan mycotoxin adsorbent were not different. It was concluded that the in vivo hepatic FSR of laying hens was inhibited by the feeding of grains naturally contaminated with Fusarium mycotoxins and that this may explain some of the adverse effects seen when contaminated grains were fed to laying hens.

Two experiments were conducted to compare the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on brain regional neurochemistry of starter pigs and broiler chickens. A polymeric glucomannan mycotoxin adsorbent (GM polymer) was also tested for its efficacy in preventing Fusarium mycotoxicoses. In Exp. 1, a total of 150 starter pigs (initial weight = 9.3+/-1.1 kg) were fed five diets (six pens of five pigs per diet) for 21 d. Diets (as-fed basis) included control, 17% contaminated grains, 24.5% contaminated grains, 24.5% contaminated grains + 0.2% GM polymer, and a pair-fed control for comparison with pigs receiving 24.5% contaminated grains. In Exp. 2,360 1-d-old male broiler chicks were fed for 56 d one of four diets containing the same source of contaminated grains as was fed to pigs. The diets included control, 37% contaminated grains, 58% contaminated grains, and 58% contaminated grains + 0.2% GM polymer (as fed). Neurotransmitter concentrations in the cortex, hypothalamus, and pons were analyzed by HPLC. The following brain neurotransmitter alterations (P < or = 0.05) were observed. In pigs, inclusion of contaminated grains in the diet 1) linearly increased cortex 5-hydroxytryptamine (5HT, serotonin) concentrations, while linearly decreasing hypothalamic tryptophan concentrations; 2) quadratically increased hypothalamic and pons 5-hydroxyindoleacetic acid (5HIAA):5HT ratios, whereas the ratio decreased linearly in the cortex; and 3) linearly increased the ratio of hypothalamic 3,4-dihydroxyphenylacetic acid:dopamine (DA) concentrations, whereas hypothalamic norepinephrine (NRE) and pons DA and homovanillic acid (HVA) concentrations linearly decreased. In broiler chickens, inclusion of contaminated grains in the diet 1) linearly increased concentrations of 5HT and 5HIAA in the pons and 5HT concentrations in the cortex; 2) linearly decreased 5HIAA:5HT ratio; and 3) linearly increased pons NRE, 3-methoxy-4-hydroxyphenylethylene glycol, DA, and HVA concentrations. Supplementation of GM polymer to the contaminated diet decreased (P < 0.05) 5HT and 5HIAA concentrations in the cortex of pigs. It was concluded that the differences in alterations of brain neurochemistry might explain the species differences in the severity of Fusarium mycotoxin-induced feed refusal.

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.

The effects of trichothecene nivalenol (NIV) on the health and production of laying hens were determined in a feeding study. White Leghorn hens, 55 weeks old, were fed diets containing 0, 1, 3 and 5 mg NIV/kg during 50 days. Feed intake was reduced by NIV, but there were no effects on body weight, egg production and egg quality. Traces of unaltered NIV were found in liver and bile. Alkaline phosphatase in the blood plasma increased in the hens fed 0, 1 and 3 mg NIV/kg diet but decreased in the birds fed 5 mg NIV/kg feed. Total protein and glucose were slightly reduced in hens fed 5 mg NIV/kg diet. Pathological examination revealed that 40-75% of hens fed NIV (3 and 5 mg/kg) supplemented diet showed gizzard lesions, haemorrhages in the duodenum and swollen cloaca and oviducts with immature eggs while certain birds in the 1 mg NIV group showed light and fragile livers. NIV and the metabolite de-epoxy-NIV in faeces were found to constitute up to 10% of ingested NIV.

Three experiments were conducted to determine the effects of 4,15-diacetoxyscirpenol (DAS) on egg quality and egg production of broiler breeders. In Experiment 1, feed containing 0, 1.25, 2.5, or 5.0 mg DAS/ kg was fed from 67 to 69 wk of age followed by a 3-wk recovery period on a slat-litter floor. In Experiment 2, individually caged broiler breeder females were studied from 23 to 31 wk of age. The basal diet containing 0, 5, 10, or 20 mg DAS/kg was fed from 25 to 27 wk of age. In Experiment 3, individually caged broiler breeder hens were studied from 23 to 32 wk of age. DAS was fed at levels of 0 (basal), 5, 10, and 20 mg DAS/kg for 2 wk beginning at Week 24, followed by the basal breeder diet for 7 wk. Egg production was not affected by levels of up to 5 mg DAS/kg in the older hens of Experiment 1. When fed from 25 to 27 wk of age in Experiment 2, DAS decreased egg production at the 20 mg/kg level only. When fed from 24 to 25 wk of age in Experiment 3, DAS had no significant effect on egg production or egg quality. Short-term consumption of DAS at levels that might naturally occur appears to have little effect on broiler breeder egg production.

16-wk experiment with laying hens was carried out to examine the effects of feeding of mycotoxin-contaminated maize (CM) on performance, nutrient digestibility, weight of organs, serum chemical parameters, and antibody titers to Newcastle disease virus (NDV) in serum. Also tested were fimbrien antigen K88 in egg yolk and zearalenone (ZON) residues in eggs and tissues. The Fusarium-toxin-contaminated maize contained 17,630 microg deoxynivalenol and 1,580 microg ZON/kg. Moreover, Mycofix Plus (MP), a so-called detoxifying agent, was added to both the uncontaminated control (UCM) and to the CM diet (70% dietary maize inclusion). Each of the four resulting diets (UCM, UCM-MP, CM, CM-MP) was tested on 25 laying hybrids (Lohmann Brown). Feeding of the CM diets significantly depressed feed intake compared to the control groups by approximately 5%. This was mainly due to the effects observed at the beginning of the experiment. Daily egg mass production/hen was 56.6, 58.4, 53.9, and 55.2 g in groups UCM, UCM-MP, CM and CM-MP, respectively. Nutrient digestibility and metabolizability of gross energy were slightly depressed by feeding the CM diets and improved by MP addition. Feeding of the CM diets resulted in a significant decrease in serum titers to NDV and to an increase in yolk titers to antigen K88. No residues of ZON or of its metabolites were found in yolk, albumen, abdominal fat, breast meat, follicles greater than 1 cm in diameter, ovaries including follicles smaller than 1 cm in diameter, magnum, and serum. ZON and alpha-zearalenol (alpha-ZOL) were detected in livers of hens fed the CM diets at mean concentrations of 2.1 and 3.7 microg/kg, respectively. It was concluded that feeding maize which was highly contaminated with Fusarium mycotoxins adversely influenced performance of hens and modulated immune response. At the given level of zearalenone and at the indicated detection limits, no residues of ZON and its metabolites were found in eggs. The effects of the tested detoxifying agent were quite mycotoxin-independent.

Unlabelled: Aflatoxin (AF) and clinoptilolite (CLI, a natural zeolite) were added to broiler food and some biochemical values and enzyme activities were evaluated. The experimental design consisted of six dietary treatments. (1), Control: basal diet; (2) CLI: basal diet plus 15 g clinoptilolite kg(-1) diet; (3) 50 ppb AF: basal diet plus 50 microg total aflatoxin (AF; the composition given below) kg(-1) diet; (4) 50 ppb AF+CLI: basal diet plus 50 microg AF plus 15 g CLI kg(-1) diet; (5) 100 ppb AF: basal diet plus 100 microg AF kg(-1) diet; (6) 100 ppb AF+CLI: basal diet plus 100 microg AF plus 15 g CLI kg(-1) diet. A commercially available CLI was provided from the west region of Turkey and its chemical formula is "KNa(2)Ca(2)(Si(29)AL(7))O.7(2).32H(2)O". For this a total of 576 1-day-old Ross broiler chicks were housed in six treatment groups from days 1 to 42. AF treatment significantly increased the serum Na levels and the aspartate-amino-transferase (ASAT) and alanine-amino-transferase (ALAT) enzyme activities, while total protein, albumin, total cholesterol uric acid, and K levels were not significantly different between groups. These results suggest that these low AF levels in food did not change the serum biochemistry but significantly affected the enzyme activities in broilers.

Three hundred sixty, 1-d-old male broiler chicks were fed diets containing grains naturally contaminated with Fusarium mycotoxins for 56 d. The four diets included control (0.14 mg/kg deoxynivalenol, 18 mg/ kg fusaric acid, < 0.1 mg/kg zearalenone), low level of contaminated grains (4.7 mg/kg deoxynivalenol, 20.6 mg/kg fusaric acid, 0.2 mg/kg zearalenone), and high level of contaminated grains without (8.2 mg/kg deoxynivalenol, 20.3 mg/kg fusaric acid, 0.56 mg/kg zearalenone) and with (9.7 mg/kg deoxynivalenol, 21.6 mg/kg fusaric acid, 0.8 mg/kg zearalenone) 0.2% esterified-glucomannan polymer derived from Saccharomyces cerevisiae1026 (E-GM). Body weight gain and feed consumption responded in a significant quadratic fashion to the inclusion of contaminated grains during the finisher period. Efficiency of feed utilization, however, was not affected by diets. The feeding of contaminated grains in the finisher period also caused significant linear increases in blood erythrocyte count and serum uric acid concentration and a significant linear decline in the serum lipase activity. Dietary inclusion of contaminated grains resulted in a significant quadratic effect on serum albumin and y-glutamyltransferase activity. Blood hemoglobin and biliary IgA concentrations, however, responded in significant linear and quadratic fashions. Supplementation of E-GM counteracted most of the blood parameter alterations caused by the Fusarium mycotoxin-contaminated grains and reduced breast muscle redness. It was concluded that broiler chickens may be susceptible to Fusarium mycotoxicoses when naturally contaminated grains are fed containing a combination of mycotoxins.

Beginning at 24 wk of age, control diets or diets containing 50 or 100 mg/kg moniliformin (M), 100 or 200 mg/kg fumonisin B1 (FB1), or a combination of 50 mg M and 100 mg FB1/kg of diet were fed to White Leghorn laying hens for 420 d. The hens were then fed the control diet for an additional 60 d. At the beginning of the experiment, each treatment consisted of four replicates of six hens. Egg production was reduced by approximately 50% by the end of the second 28-d laying period and remained at approximately this level for the 420 d in only the hens fed the diet containing 100 mg M/kg feed. Production returned to control levels or above within 60 d after hens were fed the control diet. Egg weights were reduced by the 100-mg M diet during the first three 28-d laying periods before returning to weights comparable with controls. The hens in this group also had significantly lower body weights than the other treatments. Mortality was minimal except in hens fed the 100 mg M/kg diet and the 100 mg FB1/kg diet, on which approximately 20% of the hens died. The hens were artificially inseminated with semen from males fed control diets, and fertility was not affected by the dietary treatments. Importantly, toxic synergy between M and FB1 was not observed for any of the parameters measured. Results indicate that laying hens may be able to tolerate relatively high concentrations of M and FB1 for long periods of time without adversely affecting health and performance. Interestingly, hens fed the 100-mg M/kg diet were able to recover when returned to control diets. The likelihood of encountering M or FB1 at these concentrations in finished feed is small.

Eleven-day-old chickens received 10(8) colony-forming units Salmonella typhimurium orally for 2 consecutive days. The next day, the 13-day-old chickens were given a high dose of ochratoxin A (3 mg/kg) orally. The number of S. typhimurium in both the duodenal and cecal contents of chickens administered with high doses of ochratoxin A increased significantly when compared with control birds. Ochratoxin A was shown to be one of numerous factors that affect the susceptibility of chickens to salmonellae colonization.

Electrocardiography was used to examine the acute cardiotoxic effects of moniliformin on 3-week-old broiler chickens. Each of the seven pairs of anesthetized birds (pentobarbital sodium, 40 mg/kg body weight, intramuscular) was injected intravenously with moniliformin (1 mg/kg body weight) or an equal volume of normal saline (1 ml/kg body weight), and changes in electrocardiogram were monitored for 50 minutes. Three of the seven birds injected with moniliformin died within 50 minutes post-injection. Moniliformin caused a bradycardia, which became highly significant (P < 0.05) within 15 minutes post-injection. The P-R, Q-T, and S-T intervals of moniliformin-injected birds were significantly lengthened throughout the 50-minute observation (P < 0.05). The results indicate that the moniliformin-induced mortality is due primarily to cardiac failure.

Two hundred twenty-eight male broiler chicks (Columbia x New Hampshire) were given feed amended with autoclaved culture material of Fusarium proliferatum containing fumonisin B1 (FB1) at 61, 193, and 546 ppm, fumonisin B2 (FB2) at 14, 38, and 98 ppm, and moniliformin at 66, 193, and 367 ppm in 3 separate feeding trials (amounts of toxin in each trial, respectively). Birds were started on amended rations at days 1, 7, and 21 and continuing for 14 days. Of serum chemistry parameters, only glucose was significantly decreased. Significant increases were noted in serum cholesterol, sodium, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and gamma-glutamyl transferase. Of the hematologic parameters, significant decreases were noted in red blood cell counts, hemoglobin, packed cell volume, and white blood cell counts. Immunologic changes included impaired anti-Newcastle disease antibody hemagglutination inhibition titers associated with relative decreases in total serum globulins and increases in albumin/globulin ratios. The changes were noted in all treatment groups when compared to controls.

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.

The toxicity of Fusarium proliferatum M-7176 cultured on corn (FPC) and nutritional intervention were investigated in baby chicks (New Hampshire x Single Comb White Leghorn) in three 2-wk feeding experiments. In Experiment 1, 30% FPC decreased weight gain (P < .05) and increased relative heart weight (RHW) (P < .01). Experiment 2 included a 2 x 2 factorial arrangement of FPC (0 or 30%) and Se (0 or 5 mg/kg) and two detached treatments of Se (2.5 mg/kg) or thiamin (B1, 25 mg/kg) supplementations to 30% FPC. Only B1 was inhibitory to the toxic effects of FPC on weight gain, feed efficiency, and RHW (P < .05). Experiment 3 included 2 x 2 factorial arrangement between FPC (0 or 30%) and Se (0 or 4 mg/kg), or B1 (0 or 50 mg/kg), or vitamin E (0 or 50 IU/kg) and additional supplementations of Se (2 mg/kg), B1 (10 or 25 mg/kg), or E (10 IU/kg) to 30% FPC. A new batch of FPC was used and it caused 36% mortality. Vitamin E did not interact with FPC, but SE interacted with FPC only on RHW (P < .01). Thiamin interacted with FPC on all measured variables with significance ranging from P < .1 to P < .01. Supplementation of B1 as low as 10 mg/kg was inhibitory to some toxic effects of FPC. However, B1 as high as 50 mg/kg did not completely negate the cardiotoxicity. Water-extractable B1 in FPC diets was 13 to 27% of the control diets. Water extract of FPC reduced B1 recovery from a standard solution by 40%. The anti-thiamin factor was heat-sensitive. Both fumonisins and moniliformin were present in FPC. However, the results indicate that the anti-thiamin factor is also a major toxic factor of F. proliferatum M-7176.

Chicks were fed for 3 weeks a practical broiler starter diet amended with fusarochromanone (FC), a mycotoxin. In Hubbard broiler chicks, the highest test dose of FC (75 ppm) suppressed body weight by 33% and humoral response to sheep erythrocytes by 34% to 50%, and increased the incidence of tibial dyschondroplasia (TD) to 100%. The intermediate dose (35 ppm) significantly increased the incidence of TD in both types of broiler chicks (Hubbard and Indian River), but its effect on humoral response to sheep erythrocytes was not consistent across several experiments. A minimum dietary concentration greater than 20 ppm was required to significantly increase the incidence of TD. Excessive dietary copper or zinc (200 ppm) alleviated the effect of FC on TD. However, activities of copper-dependent ceruloplasmin and superoxide dismutase was not affected by FC. Cartilage mineral profiles in FC- or Thiram-induced TD differed from that of 1-day-old hypertrophic embryonic cartilage core (less K and Mn). FC did not induce TD in leghorn chicks.

Cyclopiazonic acid dissolved in corn oil was administered by gavage to broiler chicks (n = 80) daily, from the day of hatching for 23 days. Chicks were assigned to 3 groups (1, 2, or 4 mg of cyclopiazonic acid/kg of body weight); a control group was given corn oil. Each group was composed of 10 male and 10 female chicks. Surviving chicks were euthanatized and necropsied on day 24. Histologic examination revealed that the most common lesions consisted of necrosis and hemorrhage or hyperplasia of the mucosa of the proventriculus and hepatocellular vacuolation. Skeletal muscle degeneration, characterized by myofiber swelling or fragmentation accompanied by an infiltrate of macrophages and heterophils, was detected in the group given 4 mg/kg. This degeneration was associated with an increase of plasma creatine kinase activity. Focal hepatocellular and splenic necrosis also developed in the groups given 4 mg/kg.

Citrinin is a nephrotoxic mycotoxin produced by common molds. Previous research has shown that citrinin causes increased urine flow, increased free water clearance, and increased sodium, potassium, and inorganic phosphate excretion. The present study was conducted to evaluate the dose-response effects of citrinin and to further evaluate previously reported phosphaturic effects of citrinin. Ureteral urine was collected from anesthetized domestic fowl during a control period (30 min) and during unilateral renal portal infusion (90 min) of citrinin carrier vehicle, 200 ppm citrinin, or 400 ppm citrinin. Comparisons of the portal infused vs. uninfused kidneys were used to evaluate the direct effects of citrinin. Citrinin caused acute (unilateral) dose-related increases in urine flow, free water clearance, and fractional sodium excretion and dose-related decreases in urine osmolality. Citrinin had no direct effect on glomerular filtration rates, fractional potassium excretion, or fractional inorganic phosphate excretion. An additional group of birds received systemic intravenous infusions of parathyroid hormone (PTH) beginning 40 min after the start of unilateral renal portal infusion of citrinin. The citrinin and PTH infusion were continued for 60 min. Fractional inorganic phosphate excretion increased bilaterally during the citrinin-PTH infusion period but citrinin had no direct phosphaturic effect. Previously reported phosphaturic effects of citrinin were not confirmed in the present study.