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* Department of Animal and Poultry Science,
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Department of Human Biology and Nutritional Sciences, and
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Department of Biomedical Sciences, University of Guelph, Guelph, ON N1G 2W1, Canada, and
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Department of Pharmacology and Toxicology, University of Kuopio, Fin-70211 Kuopio, Finland
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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-glutamyltransferase activities responded in a quadratic fashion (P = 0.02). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were decreased in pigs fed the diet containing the high level of contaminated grains. The feeding of contaminated diets did not significantly alter organ weights expressed as a percentage of BW, serum immunoglobulin concentrations, percentages of peripheral blood lymphocyte subsets, contact hypersensitivity to dinitrochlorobenzene, or primary antibody response to sheep red blood cells (P > 0.05). It was concluded that most of the adverse effects of feeding Fusarium mycotoxin-contaminated grains to starter pigs were caused by reduced feed intake. Although supplementation of GM polymer to the contaminated diet prevented some toxin-induced changes in metabolism, it did not prevent the mycotoxin-induced growth depression under the current experimental conditions.
Key Words: Fursaric Acid • Fusarium • Immune Response • Mycotoxins • Pigs • Vomitoxin
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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). Fusaric (5-butylpicolinic) acid (FA), a nontrichothecene mycotoxin produced by many Fusarium fungi (Bacon et al., 1996), can synergistically increase the toxicity of DON in pigs (Smith et al., 1997). Increased brain serotonergic activity and serum immunoglobulin (Ig) concentrations have been observed in pigs fed grains contaminated with DON, FA, zearalenone, and 15-acetyldeoxynivalenol (Swamy et al., 2002b). Supplementation of mycotoxin-contaminated diets with a polymeric glucomannan mycotoxin adsorbent (GM polymer) was able to prevent some of these changes (Swamy et al., 2002b). This adsorbent binds mycotoxin molecules in the intestinal lumen and prevents their up take into blood and transport to target tissues.
Little research has been conducted with respect to the effect of feeding grains naturally cocontaminated with DON and other Fusarium mycotoxins on the immune response of pigs. Reduced or delayed antibody response to thymus-dependent antigens was observed in growing pigs fed DON-contaminated grains (Rotter et al., 1994; Overnes et al., 1997). Identification of any changes in lymphocyte subpopulations and cytokines associated with these effects on the antibody response would be of interest. The need for differentiating the systemic toxicity of Fusarium mycotoxins from their feed refusal effect, moreover, has been emphasized, especially when immune response parameters are studied (Rotter et al., 1994). An experiment was conducted, therefore, to investigate the effects of feeding a blend of grains naturally contaminated with Fusarium mycotoxins on appetite suppression, growth, and immunological parameters of starter pigs. The efficacy of dietary supplemental GM polymer in preventing Fusarium mycotoxin-induced adverse effects was also determined.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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The experiment consisted of six blocks with time as the basis for blocking. In each block, pigs in a pen were fed one of five diets for 22 d. The control diet (Table 1) was formulated to meet all nutritional requirements of 8- to 20-kg starter pigs (NRC, 1998). The mycotoxin-contaminated diets (Table 1) were formulated by replacing control corn and wheat with corn and wheat naturally contaminated with Fusarium mycotoxins.
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Analysis of Dietary Mycotoxins
Dietary contents of DON, 3-acetyldeoxynivalenol, 15-acetyldeoxynivalenol, nivalenol, T-2 toxin, iso T-2 toxin, acetyl-T-2 toxin, HT-2 toxin, T-2 triol, T-2 tetraol, fusarenon-X, diacetoxyscirpenol, scirpentriol, 15-acetoxyscirpentriol, neosolaniol, zearalenone, and zearalenol were analyzed using gas chromatography-mass spectrometry (North Dakota State University, Fargo, ND) (Table 2). The detection limit for these mycotoxins was 0.2 ug/g. Dietary FA content was determined according to Matsui and Watanabe (1988), as modified by Smith and Sousadias (1993), and confirmed by Porter et al. (1995).
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Organ Weights.
On d 21 of the experiment, 12 pigs per treatment (two per pen) were killed by injection of 5 mL of Euthansol (pentobarbital sodium, 340 mg/mL, Schering Canada Inc., Pointe Claire, Quebec, Canada) into the heart followed by decapitation. Liver, kidney, and spleen were excised and weighed. Organ weights were expressed as percentage of BW.
Blood Collection.
Blood was collected from the retro-orbital sinus of 12 pigs per treatment (two per pen). On d 7, one set of blood samples was collected in heparinized vials for hematology determinations, and another set was collected in vials without anticoagulant to collect sera for serum chemistry. Serum Ig analyses were performed on d-21 serum samples, whereas hematology and phenotyping of peripheral blood lymphocyte subpopulations was performed on d-22 whole blood samples (12 per treatment). Aliquots of serum for measuring Ig and antibody titers were frozen at -80°C until analyzed.
Hematology, Serum Chemistry, and Serum Immunoglobulins.
Serum concentrations of total protein, albumin, globulin, glucose, ß-hydroxybutyrate, haptoglobin, urea, cholesterol, creatinine, bilirubin, calcium, phosphorus, magnesium, sodium, potassium, chloride, and activities of alkaline phosphatase, glutamate dehydrogenase, aspartate aminotransferase, -glutamyltransferase, and creatine kinase were determined using a Hitachi 911 autoanalyzer (Roche Diagnostics, Division of Hoffmann-La Roche Limited, Quebec, Canada). Red blood cell count, mean corpuscular volume, and hematocrit were determined and mean corpuscular hemoglobin and mean corpuscular hemoglobin concentrations were calculated. Hemoglobin was measured as cyanomethemoglobin after lysing the red blood cells using an Advia 120 Hematology System (Bayer Inc., Healthcare Division, Toronto, ON, Canada). Complete blood cell counts (differential leukocyte count) were performed manually. Serum IgM, IgG, and IgA concentrations were measured according to Swamy et al. (2002b).
Antibody Response to Sheep Red Blood Cells.
Eight days after exposure of pigs to experimental diets, preimmune sera were collected from 12 pigs per treatment followed by i.v. injection of 1 mL of 10% sheep red blood cells (SRBC) in PBS. Serum was collected subsequently on d 15 and 22. Serum IgM and IgG antibody titers specific to SRBC were measured according to Temple et al. (1995) with some modifications. Horseradish peroxidase (HRP)-conjugated goat anti-pig IgM (µ-chain specific) and IgG (-chain specific) (KPL, Gaithersburg, MD) antibodies were used as detection antibodies. The antibody titer was defined as the highest dilution of the test serum whose absorbance was greater than the average absorbance plus three standard deviations of eight serum control wells at an optical density of 405 mm. Titers were expressed as the reciprocal of base 2 log values.
Phenotyping of Peripheral Blood Lymphocytes.
Blood (10 mL) was mixed with 20 mL of Dulbecco’s PBS (D-PBS) and then underlayed with 7 mL of Lympholyte-Mammal (Cedarlane, Hornby, ON, Canada) for density gradient separation of peripheral blood mononuclear (PBMN) cells. The blood samples were centrifuged at 400 x g at room temperature for 30 min. The cell layer at the Lympholyte interface was transferred, washed 3x with D-PBS, and suspended in 1 mL of D-PBS. The total number of PBMN cells was calculated and based on trypan blue dye exclusion; cell viability was consistently >95%.
Fifty microliters of the suspended PBMN cells (1 x 106 cells) were transferred to a 96-well round-bottomed plate, followed by the addition of 50 µL of the appropriate antibody (Cedarlane, Hornby, ON, Canada). Cells were dual stained with 5 µg of unconjugated mouse anti-porcine cluster designation-determinant 4 (CD4) monoclonal antibody (clone MIL17, IgG2b isotype) and 5 µg of mouse anti-porcine CD8 monoclonal antibody conjugated to fluorescein isothyocyanate (clone MIL-12, IgG2a isotype) to label CD4+ and CD8+ T cells, respectively. Rabbit anti-mouse IgG polyclonal antibody conjugated to phycoerythrin was used as a secondary antibody to stain CD4+ T cells. B-lymphocytes were labeled with 50 µg of fluorescein isothyocyanate conjugated goat anti-porcine IgM (heavy chain specific) polyclonal antibody (IgG isotype). Appropriate isotype controls were included in the analysis and were subtracted from the sample values. The plate was shaken manually for 15 s at the outset and incubated at 4°C for 30 min in the dark for each step of antibody labeling. The plate was subsequently washed three times with D-PBS containing 1% BSA. Cells were suspended at the end in 500 µL of the DPBS-BSA and analyzed by flow cytometry using an Epics XL-MCL flow cytometer (Beckman-Coulter, Mississauga, Canada). Each analysis, including those of negative control samples, was based on 25,000 events after dead cells and residual erythrocytes were eliminated by gating on the basis of forward angle light scatter and, after residual blood polymorphonuclear cells were eliminated by gating on 90° light scatter.
Contact Hypersensitivity Response to Dinitrochlorobenzene.
This procedure was performed according to Mallard et al. (1989) with some modifications. A 5% (wt/vol) solution of 1-chloro-2,3-dinitrobenzene (DNCB, Sigma, St. Louis, MO) in 95% ethanol was mixed with an equal volume of dimethyl sulfoxide (Fisher Scientific, Ottawa, ON, Canada). Twelve pigs per treatment (eight male and four female pigs) were sensitized on d 8 of the experiment by application of 100 µL of this solution to the skin surface on the dorsal aspect of the neck. Initial thickness of the skin fold at the dorsal aspect of the base of both ears was measured on d 20 of the experiment and 200 µL of 1% DNCB in 4:1 acetone and olive oil (challenge dose) was topically applied onto the base of the right ear. Negative control sites (base of the left ear) received 200 µL of 4:1 acetone and olive oil. Irritancy control pigs (total number of 6) were not sensitized with DNCB, but were challenged similarly to test animals. Twenty-four and 48 h after the challenge with DNCB, the change in the thickness of the skin fold was measured using Harpenden calipers, and the percentage increase in thickness was calculated using the following formula (Furesz et al., 1997):
% = { [{test site thickness at 24 or 48 h - test site thickness at 0 h)/test site thickness at 0 h] - [(control site thickness at 24 or 48 h - control site thickness at 0 h)/control site thickness at 0 h]} x 100
Statistical Analyses
Data were subjected to Levene’s homogeneity of variances test before the analysis for treatment differences. Data were analyzed by analysis of covariance (initial body weight as the covariate for production parameters) or by ANOVA (for other parameters) using the GLM procedure of SAS (SAS Inst., Inc., Cary, NC) as a completely randomized block design with subsamples. Each pen with a group of five pigs was an experimental unit. Orthogonal polynomial contrasts were used to determine the nature of the response exhibited by different parameters to the feeding of graded levels of mycotoxin-contaminated grains. The pigs fed the control diet were compared with pair-fed pigs to determine the effect of feed refusal-induced nutrient deficiency on the parameters. The pair-fed pigs were tested against pigs fed the diet with a high level of contaminated grains to study toxicity of Fusarium mycotoxins other than the feed refusal. The ability of the GM polymer to prevent Fusarium mycotoxin-induced effects was also tested by a simple contrast between the pigs fed the diets containing a high level of contaminated grains with and without 0.20% GM polymer (Kuehl, 2000). Statements of statistical significance were based on P < 0.05.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionImplicationsLiterature Cited |
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). Cumulative weight gains were linearly decreased as the level of contaminated grains in the diet increased (P < 0.0001). Weight gain, however, recovered during wk 3 (P > 0.05). Growth recovery coincided with the linear increase in feed efficiency (P = 0.0004). Pigs fed the restricted amount of control diet had lower weight gains as compared to those fed control diet ad libitum (P < 0.0001). There was no difference between the pair-fed group and the pigs fed the diet containing 24.5% contaminated grains in terms of weight gain or feed efficiency (P > 0.05). The supplementation of GM polymer to the diet containing 24.5% contaminated grains did not result in improvement in feed intake or weight gain (P > 0.05). The gain:feed ratio, instead, was significantly lower in GM polymer group compared with those fed the diet containing 24.5% contaminated grains during d 14 to 21 (P = 0.01) and d 0 to 21 (P = 0.005).
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Serum Chemistry
Feeding of graded levels of contaminated grains to pigs linearly increased serum albumin-to-globulin ratio (P = 0.01), whereas serum urea concentrations and -glutamyltransferase activities responded in a quadratic fashion (P = 0.02) (Table 4). When compared with the pair-fed pigs, serum concentrations of total protein (P = 0.01) and globulin (P = 0.02) were reduced in pigs fed the diet containing 24.5% contaminated grains. Serum conjugated bilirubin (P = 0.01) and total protein (P = 0.04) concentrations were higher, whereas creatinine kinase activities (P = 0.03) were lower in pair-fed pigs as compared to pigs fed control diet ad libitum.
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Hematology
Absolute numbers of lymphocytes in the peripheral blood of pigs were linearly increased with the inclusion of contaminated grains on d 7 of the experiment (P < 0.05, data not shown). These changes, however, were not detectable on d 21 (P > 0.05, data not shown). Other leukocyte subpopulations, hematology, and serum chemistry were not affected by the dietary treatments (P > 0.05, data not shown).
Phenotype of Lymphocytes
The feeding of contaminated diets to pigs did not affect the percentage of CD4+CD8-, CD4-CD8+, and CD4+CD8+ T-lymphocytes and B-lymphocytes in the peripheral blood (P > 0.05, Table 5). Pair-fed pigs had lower percentage of CD4+CD8- cells than those fed the diet containing 24.5% contaminated grains (P = 0.02). Representative flow cytometric histograms are shown in Figure 1.
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). No significant effects of other dietary treatments, however, were noticed on skin thickness (P > 0.05).
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). Postimmune sera titers were, therefore, statistically analyzed using preimmune sera titer as covariate. There was no effect of diet on the IgM- and IgG-antibody titers to SRBC (P > 0.05).
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Discussion |
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). The concentration of FA in the contaminated diets had increased gradually as the level of inclusion of contaminated grains increased, whereas its concentration in the GM polymer supplemented diet was lower than expected. It was intended to achieve relatively lower concentrations of DON in the contaminated diets of the current study (2 ppm in diet Low and 3 ppm in diet High) as compared to Swamy et al. (2002b). Actual analysis, however, showed much higher concentrations of DON (3.9 ppm in diet Low and 5.8 ppm in diet High). This may have been due to uneven distribution of mycotoxins in the grain and the limitations of mixing. Davis et al. (1980) described the problems associated with surveying, sampling, postcollection handling, and analysis of mycotoxin-contaminated grains.
Dietary concentrations of zearalenone and 15-acetyldeoxynivalenol found in the contaminated diets of the current study have been reported to not significantly affect the performance of pigs (Young and King, 1986; Rotter et al., 1992). The adverse effects associated with the contaminated diet in the current experiment, therefore, were probably due to a combination of DON, FA, and any other unidentified Fusarium mycotoxins. The synergistic interaction between DON and FA was discussed in detail in Swamy et al. (2002b).
Direct and Indirect Effects of Fusarium Mycotoxins
Reduced weight gains and immune alterations are the major adverse effects of feeding diets contaminated with Fusarium mycotoxins, especially trichothecene mycotoxins, to animals. These adverse effects can be explained as the outcome of two events: 1) reduced feed intake; undoubtedly, the presence of any substance in the feed that reduces feed consumption would result in reduced availability of nutrients and a subsequent growth depression and increased susceptibility to diseases—this is referred to as an indirect effect of Fusarium mycotoxins and 2) direct effects of Fusarium mycotoxins on tissues and organs; this effect can provoke metabolic disturbances that are detrimental to the normal functioning of the animal. These can include the inhibition of tissue protein synthesis, altered nutrient absorption, cytotoxic effect on various cell types, altered apoptosis of lymphoid cells, oxidative damage, and cardiovascular toxicity (Bondy and Pestka, 2000).
When the pigs fed contaminated diets were compared with those fed control diet ad libitum, the differences observed could be due to both the direct and indirect effects of mycotoxins. This combined effect is the total effect. Direct or indirect effects can be equal to or less than the total effect. If either of these effects is greater than total effect, that additional effect can be attributed to factors other than the effect of Fusarium mycotoxins. Chavez and Rheaume (1986) made a first attempt to differentiate the direct and indirect effect of Fusarium mycotoxins and concluded that the effect of DON on BW gain was indirect, due to a depression in feed acceptability and intake, but there seemed to be no direct detrimental effect on the measured blood variables.
Rotter et al. (1994) reported lower skin temperature, better feed efficiency, more corrugated stomach, reduced 
-globulin levels, and lower antibody titers to SRBC in pigs consuming Fusarium mycotoxin-contaminated diet when compared with the pair-fed control pigs. The appearance of the stomach and antibody titers was not altered in pigs fed contaminated diet compared with pigs fed the control diet ad libitum; therefore, the above effects observed in the study of Rotter et al. (1994), in comparison with pair-fed control pigs, do not represent a direct effect of mycotoxins. These effects, however, may be related to the stress of pair feeding. The effect on skin temperature, feed efficiency, and serum -globulin levels, however, was due to the direct effect of mycotoxins.
Growth Measurements
Growth and feed intake of pigs fed the low level of contaminated grains over 21 d were reduced by 17.4 and 18.9%, respectively, whereas these factors were reduced by 27.7 and 33.3%, respectively, in the pigs fed high level of contaminated grains. These findings are similar to our earlier reports of starter pigs fed Fusarium mycotoxin-contaminated grains (Smith et al., 1997; Swamy et al., 2002b). The weight gain of pigs fed contaminated diets recovered during d 14 to 21, whereas feed intake continued to be lower compared with pigs fed the control diet. Recovered weight gains were due to better feed efficiency during d 14 to 21 for pigs fed contaminated grains. This finding indicated that the pigs adjusted to decreased feed intake by improving feed (nutrient) utilization. Although the definitive reason behind this improved nutrient utilization is not known, it was speculated that animals consuming Fusarium mycotoxin-contaminated diets adapt metabolically to reduced feed consumption by restricting peripheral blood circulation (reduced heat loss) (Rotter et al., 1994). In addition, Rotter et al. (1992) reported healthier gut mucosa in the pigs fed Fusarium mycotoxin-contaminated diets compared to those fed the control diet, and this might partly account for improved nutrient utilization. The finding that there was no significant differences in growth parameters comparing pigs fed the high level of contaminated grains and pair-fed controls is in contradiction to the findings of Rotter et al. (1994). They observed significantly higher weight gains and better feed efficiency in the pigs fed contaminated diets compared with the pair-fed controls. These authors attributed their findings to the stress of pair feeding.
Serum Chemistry
Evaluation of serum chemistry at the end of the previous study (Swamy et al., 2002b) resulted in no significant effect of feeding contaminated grains to pigs for 21 d. It was speculated that pigs might have adapted to contaminated grains by d 21. It was planned, therefore, to evaluate serum chemistry on d 7. An elevated serum albumin:globulin ratio was observed previously in pigs fed Fusarium mycotoxin-contaminated grains (Rotter et al., 1994). The increase in serum albumin:globulin ratio in that study was the result of increased serum albumin and decreased serum -globulin concentrations. In the current study, however, albumin concentrations were not altered. It is possible that DON and other Fusarium mycotoxins directly affect globulin synthesis in the liver and compromise the immune response of pigs (Rotter et al., 1994). Altered -glutamyltransferase activities and urea concentrations were earlier observed in livestock and poultry fed contaminated grains, and might indicate the Fusarium mycotoxin-induced hepatotoxicity and altered protein metabolism, respectively (Kubena et al., 1987).
Serum Immunoglobulin Concentrations
The lack of an effect of feeding contaminated grains on the serum Ig concentrations of pigs in the current study is in contrast to past work. It was previously observed that pigs fed contaminated grains had higher serum IgA and IgM concentrations compared to pigs fed the control diet (Swamy et al., 2002b). The reason for this discrepancy, however, is not known.
Hematology and Phenotype of Lymphocytes
The increased peripheral blood lymphocytes in differential leukocyte count 7 d after exposure to contaminated diets was similar to the findings of Pestka et al. (1990). Those researchers fed mice diets with 25 ppm of DON for 12 wk and observed a slight increase in the number of B cells in the Peyer’s patches and a drastic increase in the number of T cells in both Peyer’s patches and spleen. The increased T cells were largely due to increased CD4+ T cells. In the current study, the pigs adapted to the feeding of contaminated grains by d 21, by which time the lymphocyte counts were returned to the normal. Traditional differential leukocyte counting does not provide information on the effect of Fusarium mycotoxins on lymphocyte subpopulations. Flow cytometric evaluation of CD markers on PBMN leukocytes of pigs may serve as valuable adjunct in the evaluation of immunotoxic events (Cornacoff et al., 1995). The percentages of PBL subpopulations in the current study were comparable with that of Zuckermann and Husmann (1996). The percentages of CD4+CD8+ cells, however, were relatively lower in the current study. The strains of pigs were different in the two studies and this may account for the variability. Mistakes made in sample preparation (i.e., color compensation and placing the quadrant separating cursor) may also contribute to false positive CD4+CD8+ cell population. Unstained cells included IgM+-B cells, natural killer cells, and 
-T-cell receptor-positive T cells (Zuckermann and Husmann, 1996).
The failure to observe a significant effect of feeding Fusarium mycotoxin-contaminated grains on the percentage of PBL, unlike Pestka et al. (1990), may be explained by several factors: duration of exposure and DON concentrations were lower in the current study, the ability of DON to increase the number of CD4+ cells may be antagonistically reduced by FA and other unknown mycotoxins, the cardiovascular system contains approximately 2% of the total lymphocyte pool and it is unlikely that this is representative of the remaining 98% in other body compartments (Cornacoff et al., 1995), and PBL subsets may be influenced by multiple factors, including site and time of blood collection and stress (Cornacoff et al., 1995).
Contact Hypersensitivity to DNCB
The epidermal Langerhans cell and T lymphocytes play a pivotal role in contact hypersensitivity (CH) (Wang et al., 2000). To the best of our knowledge, no other studies to date have reported the effect of feeding Fusarium mycotoxin-contaminated grains on CH in pigs. Some studies have used lymphocyte blastogenic responses to mitogens as measures of cell-mediated immune response in pigs exposed to contaminated grains. Blastogenic responses of lymphocytes do not always correlate with other indicators of cell-mediated immune response, such as CH (Furesz et al., 1997). Blastogenic responses are nonspecific in nature, whereas CH is an antigen-specific response of T cells. In spite of this difference, lymphocyte blastogenic responses to mitogens have been routinely used in immunotoxicity testing because they provide important information about the capability of T and B lymphocytes to proliferate in response to receptor cross linking, which is an essential event for most immune responses (Smialowicz, 1995).
Rotter et al. (1994) reported no significant effect of Fusarium mycotoxins on lymphocyte blastogenic responses in pigs. Overnes et al. (1997), in contrast, fed graded levels of DON-contaminated oats to pigs and reported significantly higher in vitro lymphocyte proliferation responses to phytohemagglutinin. Purified FA has shown to reduce in vivo cell-mediated cutaneous response to phytohemagglutinin in broiler chickens (Chu et al., 1993). As observed in the study of Overnes et al. (1997), DON might enhance the proliferation of lymphocytes, but this may not be apparent in the CH response. Reasons for this might include that Fusarium mycotoxins affect both down-regulatory and up-regulatory lymphocytes of CH, and that DON and FA interacts antagonistically on the lymphocyte functions.
Antibody Response to Sheep Red Blood Cells
Temple et al. (1995) used ELISA to measure SRBC-specific serum IgM in mouse. To the best of our knowledge, the current study is the first to adapt this assay, with some modifications, to evaluate SRBC-specific serum IgM and IgG titers in pigs. Rotter et al. (1994) and Overnes et al. (1997) measured the antibody response to SRBC using a microplate hemolytic complement assay and a hemagglutination assay, respectively, in pigs fed Fusarium mycotoxin-contaminated grains. The dietary toxin levels in these studies were similar to the current study and exerted no effect on antibody titers. Rotter et al. (1994) claimed that the antibody titers were delayed in pigs fed 1.5- and 3-ppm DON-contaminated grains but provided no statistical basis for this claim. Reduced antibody titers to SRBC have been observed in mice administered 0.75 or 2.5 mg of DON/kg of BW per day by gavage for five consecutive weeks beginning at 21 d of age (Tryphonas et al., 1984). In contrast, Chu et al. (1993) reported elevated serum antibody titers against SRBC in broiler chickens fed 35 mg of purified FA/kg. It can be speculated, therefore, that the failure to observe an effect of Fusarium mycotoxins on the primary antibody response to SRBC in the current study might be the outcome of an antagonistic interaction between DON and FA. Overnes et al. (1997) observed a decrease in the secondary, but not in the primary, antibody response to tetanus toxoid in pigs fed Fusarium mycotoxin-contaminated wheat.
Effect of GM Polymer Supplementation
Feed efficiency during d 0 to 21 was significantly lower in pigs fed the GM polymer-supplemented diet vs. the unsupplemented contaminated diet. This might indicate that the polymer had bound to Fusarium mycotoxins and therefore prevented adaptation of pigs (improvement in feed utilization) to the presence of mycotoxins (Rotter et al., 1994). Some beneficial effects of GM polymer in preventing mycotoxin-induced alterations were reported earlier (Raju and Devegowda, 2000; Swamy et al., 2002a,b). Glucomannan polymer is an indigestible, nonnutritive, high-molecular-weight polymer. This material acts as a preventive treatment by adsorbing mycotoxin molecules in the intestinal lumen and preventing uptake into blood and transport to target tissues.
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Footnotes |
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2 Correspondence—phone: 519-824-4120 ext. 3746; fax: 519-822-7897; E-mail: tsmith{at}uoguelph.ca.
Received for publication February 12, 2003. Accepted for publication June 9, 2003.
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