Effect of acute oral doses of T-2 toxin on tissue concentrations of biogenic amines in the rat

T-2 toxin [3 alpha-hydroxy-4 beta, 15-diacetoxy-8 alpha-(3-methylbutyryloxy)-12,13-epoxytrichotec-9-ene] is an emetic Fusarium trichothecene mycotoxin known to cause lethargy, ataxia and feed refusal in economically important animals. Experiments were conducted to determine the effect of acute oral doses of T-2 toxin on tissue concentrations of neurotransmitters thought to play some role in regulation of feed consumption. Sixty-seven male weanling rats were intubated with a few grams of diet in a liquid slurry with or without 2.0 mg T-2 toxin per kilogram of body weight. At 1, 2, 4, 6, 8, 12, 24 and 48 h following dosing, rats were killed, and brains, spleens, hearts and adrenal glands were excised and analyzed for concentrations of neurotransmitters and metabolites using high-performance liquid chromatography with electrochemical detection. Administration of T-2 toxin caused increases in brain concentrations of tryptophan and serotonin at the early time intervals after dosing. Brain concentrations of dopamine increased, whereas concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) decreased at the later time interals following dosing. Concentrations of dopamine were increased in adrenal glands, whereas epinephrine concentrations decreased. Epinephrine was detected in spleen and heart after administration of T-2 toxin. It was concluded that the increase in brain indoleamines induced by T-2 toxin could contribute to feed refusal in animals suffering from T-2 toxicosis.     

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.     

Effect of feeding T-2 toxin contaminated feed on the utilisation of vitamin E in chickens

The purpose of the present study was to investigate the effect of experimental T-2 toxin load (2.35 mg/kg of feed) and vitamin E supply in the drinking water (10.5 mg/bird/day) on vitamin E levels of the blood plasma and liver in broiler chickens in a 14-day experiment. It was found that T-2 toxin load did not influence vitamin E content of the blood plasma except at day 3 after the toxin load when a moderate increase was detected in plasma vitamin E. No significant changes were found in vitamin E content of the liver. The simultaneous use of high-dose vitamin E supplementation and T-2 toxin load caused a significantly higher plasma vitamin E content but the changes were less expressed in the group subjected to T-2 toxin load. Vitamin E supply also resulted in a marked and significant increase in vitamin E concentrations of the liver on days 3 and 7 even in the T-2 loaded group, but this concentration significantly decreased thereafter. The results show that T-2 contamination of the diet has an adverse effect on the utilisation of vitamin E in broiler chickens.     

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)     

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.     

Deoxynivalenol and T-2 Toxin in Raw Feeds for Horses

In all, 72 samples of raw materials for equine feed were collected from farms located in different parts of northern Italy, and the presence of deoxynivalenol (DON) and T-2 toxin was evaluated using enzyme-linked immunosorbent assay. DON was detected in 38.9% of the samples tested, at levels ranging from 0.2 to 1.9 mg/kg. Maize was found to have the highest concentrations of DON, whereas barley was found to be the most commonly contaminated grain (73.3%). T-2 toxin was found in maize and rice bran at levels ranging from 12 to 102 μg/kg, with an overall incidence of 12.3% in the samples analyzed. In almost all the samples, T-2 toxin was found only in combination with DON. The occurrence of contamination observed in this survey, especially the presence of DON, is noteworthy. The levels detected are not very high, but even long-term exposure to low doses of these mycotoxins may represent a threat to horse health.     

Effect of clomipramine on monoamine metabolites in the cerebrospinal fluid of behaviorally normal dogs.

The tricyclic antidepressant, clomipramine, is an effective treatment for canine compulsive disorder (canine CD). This disorder is a clinical syndrome of abnormal conflict behaviors and its pathophysiology is unknown. However, because clomipramine is an effective treatment, information about the drug's neurochemical effect could enhance the understanding of canine CD. The following experiment used 6 behaviorally normal dogs to assess the effect of clomipramine (3 mg/kg, q24h, PO) on the central turnover of 3 monoamines (serotonin, dopamine, and norepinephrine) as measured by the concentrations of their respective metabolites in cerebrospinal fluid (CSF). In a randomized, placebo-controlled, AB-BA crossover experiment, cisternal CSF was taken after 1, 2, 4, and 6 wk on each treatment. No effect of clomipramine was detected. This contrasts with human studies that have suggested that clomipramine affects the concentrations of monoamine metabolites in lumbar CSF. However, those papers do not address methodological assumptions, such as (i) metabolites in CSF originate only from the brain, and (ii) concentrations of metabolites in cisternal/lumbar CSF reflect the concentrations in local areas of the brain. Notwithstanding the small sample size, our results suggest that more localized sampling techniques (e.g. microdialysis) are needed when examining the effect of drugs on central monoamine metabolites. Clomipramine's efficacy for canine CD indicates the need for neurobiological research and, to our knowledge, our study is the first of its kind in dogs. The resulting data are preliminary but they can inform optimal neurobiological studies of canine CD.     

Determination of the acute 50% lethal dose T-2 toxin in adult bobwhite quail: additional studies on the effect of T-2 mycotoxin on blood chemistry and the morphology of internal organs

Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.     

T-2毒素激活活性氧/核转录因子-κB信号通路诱导猪空肠上皮细胞发生炎性反应

本试验以猪空肠上皮细胞(IPEC-J2)为模型细胞,探讨T-2毒素诱导IPEC-J2炎性反应的影响及相关作用机制.通过四甲基偶氮唑盐(MTT)方法测定细胞活力,选择适宜的T-2毒素和N-乙酰-L-半胱氨酸(NAC)浓度.试验分为4个组,分别为对照组、NAC组(4.0 mmol/L NAC)、T-2组(4.0 ng/mL...     

昆明市奶牛部分饲料霉菌毒素污染状况调查

[目的]为掌握昆明市部分奶牛饲料霉菌毒素污染状况,采集了昆明市部分奶牛场（养殖小区）的饲用玉米面、全株玉米青贮,全混合日粮（TMR）共80 批次进行分析。[方法]采用酶联免疫吸附试剂盒测定80 批饲料中黄曲霉毒素B₁（AFB₁）、赭曲霉毒素A（OTA）,玉米赤霉烯酮（ZEN）、伏马毒素（FB₁+FB₂）、T-2毒素、呕吐毒素（DON）6 种霉菌毒素含量,超标情况按照《GB 13078—2017 饲料卫生标准》判定。[结果]玉米面中ZEN检出率88.2%,平均值为（1 047.2±935.5）μg/kg,超标率达到76.4%; DON检出率82.3%,平均值为（1 375.2±635.2）μg/kg,FB₁+FB₂+FB₃检出率35.3%,平均值为（277.4±490.9）μg/kg,AFB₁检出率为35.3%,平均值为（8.6±2.9）μg/kg;OTA、T-2毒素均未检出。TMR中DON检出率25%,平均值为（1 047.2±935.5）μg/kg,AFB₁检出率为16.7%,平均值为（2.3±1.2）μg/kg,ZEN检出率16.7%,平均值（120.1±112.6）μg/kg,均未超标;OTA、T-2毒素、FB₁+FB₂+FB₃均未检出。全株玉米青贮饲料中DON检出率47.1%,平均值为（1 375.2±635.2）μg/kg,ZEN检出率为29.4%,平均值为（142.5±191.1）μg/kg,均未超标;AFB₁、OTA、T-2毒素、FB₁+FB₂+FB₃均未检出。[结论]霉菌毒素检出率：DON>ZEN>AFB1>FB₁+FB₂+FB₃ >T-2毒素和OTA;污染程度：玉米面>全株玉米青贮>TMR。三类饲料中霉菌毒素都有不同程度的污染,其中玉米面霉菌毒素污染风险最大,在运输、存储、使用时要予以高度关注,避免造成经济损失。     

Ovine platelet function and its inhibition by T-2 toxin

Ovine platelets suspended in homologous plasma aggregated effectively in response to adenosine-diphosphate, acid-soluble collagen and aggregated moderately to serotonin and arachidonic acid. Ovine platelet aggregation, in response to each agent, was inhibited in a concentration dependent fashion by T-2 toxin. The platelet aggregates which formed in the presence of T-2 toxin appeared to be less stable than aggregates in comparable control platelet suspensions.     

The effect of administration of a single dose of T-2 toxin on blood coagulation in the rabbit.

The single intravenous administration of T-2 toxin to rabbits at a dosage of 0.5 mg per kg body weight produced an alteration in several blood coagulation parameters. The activities of factors VII, VIII, IX, X and XI were decreased by approximately 40% six hours after T-2 toxin administration. Plasma fibrinogen concentration became elevated within 24 hours after T-2 toxin exposure. Circulating platelet numbers were unaffected by T-2 toxin administration. The similarity of coagulation parameter changes induced by T-2 toxin in animals receiving daily subcutaneous injections of vitamin K (0.5 mg per kg body weight) and those in nonvitamin K supplemented animals suggests that T-2 toxin does not function as a vitamin K antagonist.     

T-2 toxin induced Salmonella Typhimurium intoxication results in decreased Salmonella numbers in the cecum contents of pigs, despite marked effects on Salmonella-host cell interactions

ABSTRACT: The mycotoxin T-2 toxin and Salmonella Typhimurium infections pose a significant threat to human and animal health. Interactions between both agents may result in a different outcome of the infection. Therefore, the aim of the presented study was to investigate the effects of low and relevant concentrations of T-2 toxin on the course of a Salmonella Typhimurium infection in pigs. We showed that the presence of 15 and 83 μg T-2 toxin per kg feed significantly decreased the amount of Salmonella Typhimurium bacteria present in the cecum contents, and a tendency to a reduced colonization of the jejunum, ileum, cecum, colon and colon contents was noticed. In vitro, proteomic analysis of porcine enterocytes revealed that a very low concentration of T-2 toxin (5 ng/mL) affects the protein expression of mitochondrial, endoplasmatic reticulum and cytoskeleton associated proteins, proteins involved in protein synthesis and folding, RNA synthesis, mitogen-activated protein kinase signaling and regulatory processes. Similarly low concentrations (1-100 ng/mL) promoted the susceptibility of porcine macrophages and intestinal epithelial cells to Salmonella Typhimurium invasion, in a SPI-1 independent manner. Furthermore, T-2 toxin (1-5 ng/mL) promoted the translocation of Salmonella Typhimurium over an intestinal porcine epithelial cell monolayer. Although these findings may seem in favour of Salmonella Typhimurium, microarray analysis showed that T-2 toxin (5 ng/mL) causes an intoxication of Salmonella Typhimurium, represented by a reduced motility and a downregulation of metabolic and Salmonella Pathogenicity Island 1 genes. This study demonstrates marked interactions of T-2 toxin with Salmonella Typhimurium pathogenesis, resulting in bacterial intoxication.     

Sodium distribution in the bovine brain

Fatal sodium intoxication can occur in many species, including cattle, and postmortem confirmation often includes brain sodium concentration determination. Published information regarding brain sodium distribution in cattle was not found in a literature review. Our study was designed to determine whether sodium is uniformly distributed throughout the bovine brain. Eight whole bovine brains were collected from adult cattle with no neurologic signs or history suggestive of sodium intoxication, and with a non-neurologic cause of death diagnosed on gross examination. Brains were divided mid-sagittally. One hemisphere of each brain was homogenized. Subsamples were obtained from the remaining hemisphere (rostral, caudal, and dorsal cerebral cortices; brainstem, thalamus, and cerebellum). Sodium concentrations of regions and homogenates were measured by inductively coupled plasma–mass spectrometry. Data were analyzed using repeated measures ANOVA with a pairwise post-test to compare mean sodium concentration of each region to mean homogenate sodium concentration. Brain sodium was not uniformly distributed; sodium concentrations in different regions of the same brain varied somewhat unpredictably. Homogenization of an entire brain hemisphere appears to be the ideal method of sample preparation to ensure accurate brain sodium concentration measurement in adult cattle.     

Role of bentonite in prevention of T-2 toxicosis in rats

Experiments were conducted to determine the effect of bentonite and nonnutritive dietary polymers on toxicity and metabolism of T-2 toxin in rats. Male weanling rats were fed diets containing 5% bentonite, anion exchange resin, cation exchange resin or vermiculite-hydrobiotite. Each diet was fed with and without 3 micrograms T-2 toxin/g of feed for 2 wk. Bentonite and anion exchange resin were the treatments most successful at overcoming growth depression and feed refusal caused by T-2 toxin. Subsequent experiments tested bentonite and anion exchange resin at 0, 2.5, 5.0, 7.5 and 10% of the diet. Bentonite fed at 10% was the most effective treatment at overcoming feed refusal and growth depression. Rats were fed 0, 5, 7.5 or 10% bentonite for 2 wk and then dosed with [3H] T-2 toxin. Urine and feces were collected for 21 h after dosing and tissues were excised for determination of residual 3H. Feeding bentonite had little effect on the fraction of the dose excreted in the urine. Significant increases in fecal excretion of 3H were shown, when the feeding of 5, 7.5 or 10% bentonite was compared with the casein-based, semi-purified control diet. Dietary bentonite had no effect on residual 3H in liver or kidney, but all concentrations of bentonite tested reduced residual 3H in muscle. More 3H was found in the digesta in the small intestine and in the wall of the intestinal tissue when rats fed 5% bentonite were compared with the controls. Intestinal transit time for rats fed bentonite diets was reduced compared with that of the controls as indicated by chromic oxide marker studies.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of some clinically significant mycotoxins on the incorporation of DNA, RNA and protein precursors in cultured mammalian cells

The effects of zearalenone (F-2), ochratoxin A and T-2 toxins on the synthesis of DNA, RNA and proteins in mouse L cells were studied. F-2 toxin inhibited protein synthesis to a lesser extent than DNA and RNA synthesis, whereas ochratoxin A inhibited the synthesis of each equally. Exposure to the toxins for 24 hours relatively reduced the synthetic ability of the cells. T-2 toxin inhibited protein and DNA synthesis in parallel but RNA synthesis to a lesser extent. Enhanced incorporation of tritiated thymidine was found when L cells were exposed to 0.4 to 0.016 ng of T-2 toxin ml-1 for 24 hours.     

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.     

Interaction of T-2 fusariotoxin and monensin in broiler chickens infected with Coccidia

Field observations suggest that coccidiosis is a common cause of death in broiler chicken flocks fed diets containing sufficient amounts of ionophore antibiotics (monensin, narasin, etc.) and contaminated with mycotoxins, particularly with T-2 fusariotoxin. To study this phenomenon, broiler chickens fed diets containing different amounts of T-2 toxin and free from monensin, or containing a preventive dose (100 mg/kg of feed) of monensin, were infected experimentally with coccidian oocysts. In all groups fed a diet containing monensin plus T-2 toxin severe clinical symptoms of coccidiosis (blood-stained faeces etc). occurred. Deaths and retarded growth depended on the toxin dose and were considerable. The body mass gain of chicks fed a diet containing monensin and T-2 toxin but not infected with coccidia was inferior to that of groups fed diets which contained either monensin or T-2 toxin (experiment 2). On the basis of these findings a negative interaction of the two compounds is assumed. This seems to be supported by the results of experiment 3, i. e. the finding that the lethal dose of narasin, a compound closely related to monensin both in chemical structure and mechanism of action, proved to be much lower (LD50 = 102 mg/kg body mass) for chickens fed a diet supplemented with T-2 toxin than for the control chickens (LD50 = 176 mg/kg body mass). The present results suggest that the feeding of diets severely contaminated with T-2 toxin may alter the anticoccidial efficacy of monensin.     

Effect of T-2 toxin on resistance to systemic Salmonella typhimurium infection of newly hatched chickens

Newly hatched chickens were treated with the trichothecene mycotoxin, T-2 toxin, during the first day of life. Control chickens were treated with other agents known to cause immunosuppression--cyclosporine, cyclophosphamide, and aflatoxin. Chickens were infected on day 6 (5 days after treatment with T-2 toxin) by intraperitoneal inoculation with Salmonella typhimurium. Blood samples were collected from treated chickens (noninfected) and used to assess the responsiveness of blood lymphocytes to T-cell or B-cell mitogens, phytohemagglutinin, or lipopolysaccharide, respectively. The T-2 toxin had a profound negative effect on the ability of the chickens to resist salmonellosis, as measured by survival. However, the toxin effect in reducing phytohemagglutinin- and lipopolysaccharide-stimulated mitogenesis, though significant (P greater than 0.05), was not severe. Our data indicate a direct effect of T-2 toxin on native resistance to systemic salmonellosis, which was not accompanied by marked alteration in T- or B-cell responses to mitogenic stimulation.     

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.