Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. III. Bobwhite and Japanese quail.

Bobwhite and Japanese quail were fed diets containing 1.25, 2.50, or 5.00 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Aflatoxin induced mortality in bobwhites during the second and third week with 1.25 ppm (10%), 2.50 ppm (30%), and 5.00 ppm (40%), and during the same period with T-2 toxin at 8 ppm (20%) and 16 ppm (22.5%). Body weights of bobwhite quail were significantly decreased by the two higher levels of aflatoxin by 2 weeks of age, and by the two higher levels of T-2 toxin by 1 week of age. In Japanese quail, only the highest level of aflatoxin and T-2 toxin reduced body weight (by 3 weeks and by 1 week of age, respectively), and even then to a much lesser extent than in bobwhites (less than 10%). Aflatoxin did not affect feed-conversion ratio (FCR) in bobwhite quail, but the two higher levels of T-2 toxin increased FCR. None of the toxins induced mortality or increased the FCR in Japanese quail. Aflatoxin increased liver weight in both bobwhite and Japanese quail. OA increased kidney weight in 3-week-old Japanese quail but had no effect on the kidney weight of bobwhite quail. Mouth lesions were progressively more severe in bobwhite quail fed increasing levels of T-2 toxin, but lesions were far less severe in Japanese quail.     

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. I. Chukar partridge

Chukar partridges were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Toxin-induced mortality was seen during the third week with 4 ppm OA (12.5%) and 16 ppm T-2 toxin (15%), compared with the mortality in control chukars fed no toxin (2.5%). Body weights were significantly decreased by the highest level of aflatoxin at 3 weeks of age, by the highest level of OA by 2 weeks of age, and by 8 and 16 ppm T-2 toxin by 1 week of age. Aflatoxin did not affect liver weight and OA did not increase kidney weight in 3-week-old chukars. There was a slight decrease in kidney weight in chukars fed 4 ppm OA; however, the decrease was related to the decrease in body weight produced by the toxin. Mouth lesions were seen at all levels of T-2 toxin fed.     

Subacute toxicity of Dietary T-2 toxin in mice: influence of protein nutrition.

The subacute toxic effects of dietary T-2 toxin (20 ppm) incorporated in semipurified diets of 8%, 12% or 16% protein, were examined in young Swiss mice after one, two, three and four weeks. Dietary T-2 toxin caused substantial reductions in growth and food consumptaion, the degrees of which were greatest in mice fed the diets of reduced protein content. T-2 toxin consistently caused similar degrees of nonregenerative anemia, lymphopenia, thymic atrophy and gastric hyperkeratosis irrespective of the dietary protein level. However, erythroid hypoplasia was temporary in mice fed T-2 toxin in the 16%-protein diet such that erythroid precursors regenerated in splenic and bone marrow and were hyperplastic after four weeks. Liver to body weight ratios of mice fed T-2 toxin in the 16%-and 12%-protein diets increased during the four week trial in comparison to control mice fed at a similar rate. These observations indicated that suppression of erythropoiesis in mice by dietary T-2 toxin was temporarty and that the interval before regeneration was prolonged by diets of reduced protein content.     

Comparison of effects of dietary T-2 toxin on growth, immunogenic organs, antibody formation, and pathologic changes in turkeys and chickens.

The effect of T-2 toxin (trichothecene mycotoxin) consumption on Broad-Breasted White turkey poults and White Leghorn chicks was studied. Groups of ten 8-day-old poults were fed rations containing T-2 at 10 ppm, 2ppm, or 0 ppm (controls) for a period of 4 weeks; a 4th group (inanition control) was fed control rations equal to the amount consumed by the group fed rations containing T-2 at 10 ppm during the previous 24 hours. A similar experimental design was used to study the effect of the toxin on 1-day-old chicks. The thymus glands of the poults given the feed containing 10 ppm were markedly decreased in size compared with thymus glands from poults in the control group, 0.182 vs 0.331 (percentage of body weight). There was no significant (P less than or equal to 0.05) decrease in thymus gland size in poults given 2 ppm or in the inanition controls. Dietary treatment did not appear to affect the size of the bursa or spleen of the poults. Histopathologic examination of thymus glands from poults given 10 ppm of T-2 revealed a depletion of cortical lymphocytes. Chicks appeared less sensitive to T-2 toxin than did the poults. There was no effect by any dietary treatment on the size of the thymus gland, bursa, or spleen of chicks. Reductions were noticed in feed efficiency and weight gain. There was no effect of T-2 toxin on agglutinating antibody formation to Pasteurella multocida bacterin.     

Subacute toxicity of dietary T-2 toxin in mice: morphological and hematological effects.

Changes in hematopoietic and lymphoid tissues of young Swiss mice fed a balanced semipurified diet containing T-2 toxin (20 ppm) were examined after one, two, three, four or six weeks. During the first three weeks of exposure of T-2 toxin, lymphoid tissues, bone marrow and splenic red pulp became hypoplastic, resulting in anemia, lymphopenia and eosinopenia. Subsequently, during continued exposure to T-2 toxin, hematopoietic cells regenerated in bone marrow and splenic red pulp and became hyperplastic by six weeks. Granulopoiesis and thrombopoiesis resumed in advance of erythropoiesis. All lymphoid tissues remained atrophic throughout the six week trial. Mice exposed to T-2 toxin also developed perioral dermatitis and hyperkeratosis with ulceration of the mucosa of the esophageal region of the stomach. These results indicated that young mice were susceptible to both the irritant and the hematopoietic-suppressive toxic effects of dietary T-2 toxin. However, supression of hematopoiesis was transient and did not lead to hematopoietic failure.     

Short-term exposure to subacute doses of aflatoxin-induced depressed mitogen responses in young mallard ducks

Mallard ducklings were fed diets containing corn naturally contaminated with mixed aflatoxins, purified T-2 toxin, or no detectable mycotoxin in two trials. The aflatoxin level used was 12 ppb in the first trial and 33 ppb in the second. T-2 was added at 2 ppm in both trials. No pathology was associated with the aflatoxin used in this study, and T-2--induced lesions were described in a previous publication. The weights of primary (thymus and bursa of Fabricius) and secondary (spleen) lymphoid organs were significantly reduced in the T-2--treated birds. The total number of viable cells recovered from the thymus was significantly reduced in aflatoxin-treated birds. The numbers of viable cells recovered from thymus, bursa of Fabricius, and spleen were all significantly reduced after treatment with T-2. In each trial, significantly lower mitogenic responses were seen to pokeweed mitogen and concanavalin A in birds fed aflatoxin or T-2, representing reduction in both B-cell and T-cell mitogenesis. Birds fed aflatoxin also had significantly reduced Escherichia coli O55 lipopolysaccharide-induced mitogenic responses. These studies indicate that subacute oral exposure to aflatoxin caused a loss of normal lymphocyte reactivity in mallard ducklings. This finding supports the hypothesis that waterfowl that ingest even small quantities of mycotoxin-contaminated waste grain are likely to be more susceptible to bacterial or viral infections.     

The effects of dietary T-2 toxin on acute herpes simplex virus type 1 infection in mice

Young male white Swiss mice were fed control diet or diet supplemented with 20 or 10 parts per million (ppm) of T-2 toxin for two or three weeks. These mice then were inoculated with herpes simplex virus type 1 (HSV-1) (9.6 x 10(6) plaque forming units) intraperitoneally. To compare the effects of T-2 toxin against a known immunosuppressive drug, cyclophosphamide was injected intraperitoneally at 150 mg/kg, 24 hours after treatment with HSV-1, into mice fed the control diet. Mice were necropsied and tissues were collected for microscopic and virologic examination. White Swiss mice which consumed a daily diet containing 20 ppm of T-2 toxin for two or three weeks were highly susceptible to HSV-1 infection and 27 of 36 (75%) died as a result of extensive hepatic and adrenal necrosis. Although HSV-1 was isolated from livers and brains of mice fed 20 ppm of T-2 toxin for two or three weeks, there was little or no inflammatory response found in the adrenals, livers, spinal cords, brains, or ganglia. The necrotizing encephalomyelitis observed in control mice was absent. High levels of dietary T-2 toxin appeared to be more immunosuppressive than cyclophosphamide because only one mouse died after treatment with HSV-1 and cyclophosphamide. Mice treated with cyclophosphamide had changes in brain, spinal cord, spleens, thymus, and bone marrow which were similar to those fed 20 ppm of T-2 toxin and infected with HSV-1, however, liver lesions were much less severe. HSV-1-infected mice on a diet with 10 ppm T-2 toxin had lesions of intermediate severity when compared with HSV-1-infected mice fed a diet with 20 ppm T-2 toxin and HSV-1-infected mice on control diets. Necrosis was less extensive in the livers and adrenals. The infrequent isolation of virus from liver and brain was consistent with the lack of intranuclear inclusion bodies and a more marked inflammatory response. Ten ppm of dietary T-2 toxin only depressed bone marrow and splenic red pulp to a mild or moderate degree. This may have enhanced the necrotizing encephalomyelitis observed in mice killed on days 6 and 8 after HSV-1 infection. Liver lesions were mild and those of the adrenals were moderate in mice fed control diet. The rare isolation of HSV-1 from the liver and brain and the findings of a moderate to severe necrotizing encephalomyelitis in these mice was consistent with an essentially functional immune system.     

Subacute toxic effects of dietary T-2 toxin in young mallard ducks.

Young Mallard ducks (Anas platyrhynchos) were fed diets containing purified T-2 toxin at levels of 20 or 30 ppm for two or three weeks. Ingestion of T-2 toxin was associated with reduced weight gain and delayed development of adult plumage. Affected ducks developed caseonecrotic plaques throughout the upper alimentary tract, especially in oropharynx and ventriculus. Several ducks also developed severe ulcerative, proliferative esophagitis and proventriculitis. Generalized atrophy of all lymphoid tissues consistently occurred. The manifestations of T-2 mycotoxicosis in Mallard ducks were mostly attributable to irritant toxicity to the alimentary mucosa. The T-2 toxin caused neither hematopoietic suppression nor a hemorrhagic syndrome in ducks. These alimentary lesions of T-2 mycotoxicosis in ducks do not resemble diseases of native waterfowl presently being recognized in routine surveillance of waterfowl mortality in Saskatchewan.     

Influence of esterified-glucomannan on performance and organ morphology, serum biochemistry and haematology in broilers exposed to individual and combined mycotoxicosis (aflatoxin, ochratoxin and T-2 toxin)

1. A study was conducted to evaluate the individual and combined effects of aflatoxin B1 (AF), ochratoxin A (OA) and T-2 toxin (T-2) on performance, organ morphology serum biochemistry and haematology of broiler chickens and the efficacy of esterified-glucomannan (E-GM), a cell wall derivative of Saccharomyces cerevisiae1026 in their counteraction. 2. Two dietary inclusion rates of AF (0 and 0.3 mg/kg), OA (0 and 2 mg/kg), T-2 (0 and 3 mg/kg) and E-GM (0 and 1 g/kg) were tested in a 2 x 2 x 2 x 2 factorial manner on a total of 960 broiler chickens from 1 to 35 d of age in an open sided deep litter pen house. 3. Body weight and food intake were depressed by all the mycotoxins, OA being the most toxic during early life. 4. Weights of kidney and adrenals were increased by AF and OA. Liver weight was increased by AF (17.8%), while OA increased gizzard weight (14.6%) and reduced bone ash content (8.1%). T-2 toxin showed no effect on these variables. 5. Serum cholesterol content was decreased and activity of serum gamma glutamyl transferase (GGT) was increased by AF and OA while serum protein content was decreased by AF. These effects were more pronounced at 21 d than at 35 d of age. Inconsistent responses were seen in the other variables: blood urea nitrogen (BUN) content, activities of serum alanine amino transferase and aspertate amino transferase. Blood haemoglobin content was depressed by AF and T-2, whereas blood coagulation time was prolonged by OA. 6. Significant interactions were observed between any 2 toxins for their additive effects on body weight, food intake, bone ash content and serum GGT activity at 21 d. Conversely, antagonistic interactions were observed among any 2 of the toxins for their effects on variables such as serum protein and serum cholesterol content. Simultaneous feeding of all 3 mycotoxins did not show increased toxicity above that seen with any 2. 7. Esterified-glucomannan increased body weight (2.26%) and food intake (1.6%), decreased weights of liver (32.5%) and adrenals (18.9%) and activity of serum GGT (8.7%), and increased serum protein (14.7%), cholesterol (21.9%), BUN (20.8%) and blood haemoglobin (3.1%) content, indicating its possible beneficial effect on mycotoxicosis in broiler chickens.     

Evaluation of two mycotoxin binders to reduce toxicity of broiler diets containing ochratoxin A and T-2 toxin contaminated grain

In order to assess ochratoxin A (OA) and T-2 toxin (T-2) binding ability of two commercial sorbents, both in vitro and in vivo trials with broilers were performed. Crude OA and T-2 extracts from contaminated grain were used to assess in vitro binding ability of two sorbents (Zeotek [Zk] and Mycofix [Mx]), by quantifying free mycotoxin through an enzyme-linked immunosorbent assay (ELISA) test. For in vivo trial, a 3 x 2 x 2 factorial arrangement was used for this experiment, being the factors: adsorbents (none, Zk, and Mx), OA (0 and 567 parts per billion [ppb]) and T-2 (0 and 927 ppb). OA and T-2 contaminated wheat and corn, respectively, were added to sorghum-soybean meal diets to meet 567 ppb of OA and 927 ppb of T-2. Mycotoxins were fed alone or combined in treatments. After 21 days, blood chemistry, gross, and histological evaluations were performed. Relative weights of liver, kidney, and bursa of Fabricius were obtained. Zk had the highest OA and T-2 in vitro binding ability (100% and 8.67%, respectively). Chickens fed OA with or without sorbents had a lower body weight and feed intake reduction. However, those birds fed T-2 were partly protected by a sorbent. Birds fed both toxins showed toxic additive effects, and no protection of any adsorbent was observed. A significant reduction in plasma proteins, albumin, and globulins was a characteristic observed in all birds fed diets with OA both with or without adsorbents. Uric acid level in blood was increased in all chickens fed OA-contaminated diets. Histological findings observed in birds fed OA-contaminated diets were necrosis of kidney tubular cells, swollen and necrotic hepatocytes, bile ducts hyperplasia, and increased diameter of proventriculus glands. In birds that received T-2 alone, only the liver, with the same kind of lesions, was affected. According to these results, it can be concluded that there is not a relation between in vitro and in vivo trials. OA toxic effects could not be counteracted by any sorbent. T-2 toxicity could be partially counteracted by an adsorbent used in this research.     

Energy and nitrogen metabolism of diseased chickens: aflatoxicosis.

1. New Hampshire chicks were fed on diets containing 0 (control), 0-7 (A), or 1-1 (B) ppm of aflatoxin B1. In two trials 1-d-old chicks were offered ad libitum the three diets for 14 d. The gaseous exchange of five chickens from each group was measured for 3 or 4 d, the same diets being fed, at 2, 3, 4 and 5 weeks of age in two series of experiments. The controls were fed at the lower intake of the two other groups. Following each series of experiments at the various ages, birds were starved for 24 h and their heat production was re-measured over the next 24 h. 2. Mortality was highest and growth and food conversion poorest where the diet with the highest aflatoxin concentration was fed. Mortality was confined to the first 2 weeks. 3. Performance of birds in the chambers was improved in the second series due to differences in food intake. It also improved with age suggesting some resistance to the toxin. 4. Mean respiratory quotient was 0-97 for fed chickens on diet B. This was significantly different from 0-92 for the two other groups. Similarly, during starvation the RQ was 0-76 compared with 0-73. 5. birds fed on diet B generally grew better, retained more nitrogen and had a better energy balance in the respiration chambers than the other two groups. Metabolisability of dietary energy was less (68.5%) for all groups at 2 to 3 weeks than when older (70%) but availability of ME was the same (71%) for all groups. 6. Heat production (kJ/kg0-75) of starved birds on diet B was significantly lower than the other two groups, while endogenous nitrogen excretion was higher. 7. Water consumption (ml/g food and g/100 g body weight) was greatest for birds on diet B. 8. Although aflatoxin in the diet substantially reduced intake there was no indication that at these reduced levels of intake, nitrogen or energy metabolism were measurably impaired.     

The effect of chronic feeding of diacetoxyscirpenol and T-2 toxin on performance,health, small intestinal physiology and antibody production in turkey poults

1. The effects of feeding T-2 toxin or diacetoxyscirpenol (DAS) at levels up to 1 ppm for 32 d on performance, health, small intestinal physiology and immune response to enteral and parenteral immunisation were examined in young poults. 2. Slight improvement in growth was observed in some groups of poults fed T-2 or DAS mycotoxins for 32 d, with no change in feed efficiency. Feeding both T-2 and DAS resulted in oral lesions which had maximal severity after 7-15 d. 3. Mild intestinal changes were observed at 32 d but no pathological or histopathological lesions were found. Both mycotoxins altered small intestinal morphology, especially in the jejunum where villi were shorter and thinner. In addition, both DAS and T-2 mycotoxins enhanced the proportion of proliferating cells both in the crypts and along the villi. Migration rates were reduced in the jejunum of poults fed T-2 toxin but did not change in the duodenum or in poults fed DAS. 4. No significant effects of T-2 or DAS were observed on antibody production to antigens administered by enteral or parenteral routes. 5. This study indicates that tricothecene toxins at concentrations of up to 1 ppm for more than 30 d influenced small intestinal morphology but did not affect growth or antibody production.     

Effects of treatment of growing swine with aflatoxin and T-2 toxin

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Immunopathological effects of experimental T-2 mycotoxocosis in broiler chicken co-infected with infectious bronchitis virus (IBV)

A total of 128 1-week-old chicks were classified into four groups; T-2 toxin fed (T-2), IBV infected (IBV), T-2 toxin fed and co-infected with IBV (T-2+IBV), and untreated (control) for a period of 6 weeks. Within their respective groups, the birds belonged to T-2 and T-2+IBV were exposed to 2 ppm of T-2 toxin contaminated feed for 6 weeks, and 0.2 ml of 10 EID(50) (10(5.69)/0.2 ml) inoculums of IBV isolate (India/LKW/56/IVRI/08) was used to challenge the chicks belonged to IBV alone and T-2+IBV groups after 3 weeks of the experiment. To study immunopathological effects, parameters such as lymphocyte stimulation indices (SI), haemagglutination inhibition, enzyme linked immunosorbant assay (ELISA), peripheral lymphocytes CD(4)(+) and CD(8)(+) analysis, and histopathological examination of lymphoid organs were done. Accordingly, SI values were significantly (P<0.05) lower in all the treatment groups as compared to control, however, the SI values of IBV infected group were significantly higher than the values in toxin fed groups. The mean HI titres to ND vaccine was significantly (P<0.05) lower in the toxin groups at all the intervals, and the antibody titres in IBV infected group were significantly (P<0.05) higher than that of T-2 toxin fed and co-infected with IBV group but were significantly (P<0.05) lower than the control at 21 (3) and 28 (10) days of toxin feeding (DTF) (days post infection (DPI)). Similarly, the mean IBV ELISA antibody titres in the toxin fed groups were significantly (P<0.01) reduced as compared with the IBV ELISA antibody titres of IBV infected but not toxin fed group, at all intervals. Peripheral CD(4)(+):CD(8)(+) ratios in T-2+IBV group and number of CD(4)(+) and CD(8)(+) peripheral lymphocytes in all treatment groups were significantly reduced as compared to the values in control birds. However, CD(4)(+):CD(8)(+) ratios of IBV infected group at 42 (21) DTF (DPI) were found significantly (P<0.05) higher than the values in control birds. Histopathologically, lymphoid organs (bursa of Fabricius, spleen, thymus, caecal tonsils and Harderian glands) showed moderate to severe necrosis (lymphocytolysis) and extensive lymphocyte depletion in all the toxin groups (T-2 and T-2+IBV groups) where the severity and extent of the lesions were more in T-2+IBV group. The findings of the present experiment revealed immunosuppressive effects of T-2 toxin and aggravated the pathology and pathogenesis of IBV infection.     

Effect of aflatoxin on the humoral and cell-mediated immune systems of the chicken.

Chickens fed 2.5 microgram of aflatoxin/g of diet from 2 to 4 weeks of age or from hatching to 4 weeks were deficient in cell-mediated immunity, as measured at 4 weeks of age by the graft-versus-host reaction. Delayed-type hypersensitive skin reactions to tuberculin were also reduced in chickens given dietary aflatoxin from hatching to 7 weeks of age. Humoral immunity, as measured by the ability of 4-week-old chicks to produce natural agglutinins to rabbit red blood cells, was not significantly altered by dietary aflatoxin. A significant decrease in concentrations of serum immunoglobulins (Ig) IgG and IgA, but no IgM, however, did occur in chicks given dietary aflatoxin from hatching to 4 weeks or between 2 and 4 weeks of age. Aflatoxin consumption from 0 to 2 weeks of age produced no marked effect on either cell-mediated or humoral immunity in 4-week-old chicks.     

Evaluation of diets contaminated with aflatoxin and ochratoxin fed to growing pigs

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical performance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.     

Economic effects of clinical chicken anemia agent infection on profitable broiler production.

An outbreak of anemia dermatitis syndrome caused by chicken anemia agent (CAA) occurred in 15 broiler flocks. An average of 29% of chickens in these flocks were derived from a common breeder flock. The breeder flock had no antibody to CAA at 20 weeks of age but had seroconverted by 31 weeks. Diseased broiler flocks were derived from eggs laid by the breeder flock between 25 and 30 weeks of age. CAA infection in the breeder flock was subclinical, with no apparent effects on mortality or performance. A strategic program of therapeutic and/or prophylactic antibiotic therapy was begun in affected broiler flocks as soon as the disease was diagnosed. Nevertheless, when the cost of therapy was taken into account, affected broiler flocks had a net income 17.3% to 19.6% lower than normal flocks. Average bird weights were 3.3% to 3.5% lower in affected flocks than in unaffected flocks, and affected flocks had a significantly greater proportion of lighter birds. Average mortality in affected flocks was 2.0% to 2.3% higher than in normal flocks, with peak mortality occurring in the third week of life. There was no apparent effect on feed-conversion ratio.     

The effects of aflatoxin on the reproductive system of roosters

This study was conducted to determine the pathological changes in testes and epididymides and plasma testosterone levels of adult roosters during experimentally induced aflatoxicosis. In the study, 24 months of age, 32 Babcock breeder males were used, and they were divided into four groups each containing 8 animals. The groups were designed as follows; group 1: Control, no aflatoxin (AF), group 2: 5 ppm (parts per million) total aflatoxin (AF; B1, B2, G1, G2), group 3: 10 ppm AF and group 4: 20 ppm AF in the diet, and the birds were fed for 8 weeks. Grossly, it was seen that the testes of all AF-treatment groups birds were significantly (P < 0.001) atrophied when compared with those of control birds. Histopathologically, there was no spermatogenesis in the testes of 4, 5 and 6 cocks fed on a diet containing AF 5, 10 and 20 ppm, respectively. Furthermore, abnormal spermatozoa were observed in some of AF-treatment groups (in 2 cases in each of 5 and 10 ppm AF-treated groups, and in one case in 20 ppm AF-treated group). There were also mononuclear cell infiltration and/or focal lymphoid cell accumulation in the intertubular areas of the testes and epididymides in all AF-treatment groups. In conclusion, it has been shown that AF might totally or partially (dose related) suppress spermatogenesis, cause abnormality in spermatozoa and atrophy in testes. Furthermore, there was degeneration and desquamation in the epithelium and decrease in the size and thickness of the germinative layer of the seminiferous tubules, and lowered plasma testosterone levels in adult roosters.     

Effect of subclinical levels of T-2 toxin on the bovine cellular immune system.

The effect of subclinical levels of mycotoxin T-2 on the cells of the bovine immune system was investigated in two in vivo experiments. In experiment 1, five calves were orally dosed with 0.3 mg/kg/day of T-2 toxin for 56 days and five calves were pair fed controls. The neutrophil function as measured by nitroblue tetrazolium reduction was reduced in the mycotoxin treated calves. The cutaneous reaction to intradermally injected phytohemagglutinin was reduced in the T-2 toxin treated calves. B-cell (SIg+) numbers increased slightly, but T-cell (PNA+) numbers were not affected during the experimental period. In the second experiment, six calves were given 0.5 mg/kg/day T-2 toxin orally for 28 days and six calves were pair fed controls. B-cell numbers and the response of a B-cell enriched fraction to phytohemagglutinin increased after toxin administration. T-cell numbers and the response of a T-cell enriched fraction and the whole mononuclear cell population to phytohemagglutinin was reduced only on day 19 posttoxin administration. The in vitro (T-2 toxin) exposure of the mononuclear cell population, B-cell enriched, or T-cell enriched fraction reduced their lymphoblastic response to mitogens. A 50% reduction was induced by as little as 1.4 ng/mL of T-2 toxin.     

Use of amprolium for the control of coccidiosis in pheasants

Amprolium administered in feed during the first 4 weeks of life at a level of 0.0175% protected pheasants against three major pathogenic species of coccidia (Eimeria colchici, E. duodenalis, and E. phasiani) when they were exposed at 2 weeks of age. The difference was significant when mortalities were compared between medicated infected (3%) and unmedicated infected (35%) pheasants. The manufacturer's proposed level (0.0175%) and twice the proposed level (0.0350%) of amprolium had no significant effect on weight gains or mortality in the safety trial. Amprolium residues found in the muscles and livers of pheasants that received either level of amprolium did not exceed the tolerance levels for chickens and turkeys permitted by the U.S. Food and Drug Administration.