Clinical and pathologic changes in acute bovine aflatoxicosis: rumen motility and tissue and fluid concentrations of aflatoxins B1 and M1

Effects of aflatoxin on bovine rumen motility were determined by radiotelemetric techniques. Aflatoxin altered amplitude and/or frequency of rumen contractions in steers given dosages of 0.2, 0.4, 0.6, or 0.8 mg of aflatoxin/kg of body weight. Effects of aflatoxin on rumen motility were dose dependent. An increase in elimination time of aflatoxin from rumen contents was observed in steers given the aflatoxin dosages of 0.4 to 0.8 mg/kg. The increase in elimination time of this toxin facilitates diagnostic capabilities for detecting bovine aflatoxicosis by obtaining rumen contents for analysis for aflatoxin. Aflatoxin M1 was detected in rumen contents from steers at 2 hours after aflatoxin was administered. Thus, intraruminal metabolism of aflatoxin B1 to M1 may occur.     

Complement activity, serum protein, and hepatic changes in guinea pigs given sterigmatocystin or aflatoxin, alone or in combination

Effects of either sterigmatocystin or aflatoxin, alone or in combination, given orally to guinea pigs were studied. Sterigmatocystin and aflatoxin B1 given alone and in combination at 4.2 mg/day and 0.01 mg/day, respectively, markedly reduced body weight. Although changes in total serum protein were not marked in any of the guinea pigs in this study, sterigmatocystin given alone and aflatoxin given alone significantly ( less than 0.05) decreased alpha2-globulin. The combination of toxins significantly (P less than 0.01) increased albumin and significantly (P less than 0.01) decreased both alpha2- and beta-globulins. Sterigmatocystin depressed complement activity, although not significantly. However, the combination of sterimatocystin with 0.01 mg of aflatoxin B1/day (an amount that does not affect complement activity alone) significantly (P less than 0.01) reduced complement activity. Increased severity of lesions was not found in guinea pigs given aflatoxin at 0.01 mg of B1 equivalents/day in addition to the sterigmatocystin.     

Effects of xanthene dyes in cattle diets for insect control: diet digestibility and fecal excretion

The effects of rose bengal, erythrosin B and fluorescein on ruminant digestion were evaluated by an in vitro rumen technique. Rose bengal reduced in vitro dry matter disappearance (IVDMD) values starting at .5 mM in the nutrient media and erythrosin B reduced IVDMD values starting at .05 mM in the nutrient media. Maximum reduction in IVDMD values was observed at 3.0 mM of rose bengal and erythrosin B. Fluorescein depressed digestion but not as severely as rose bengal or erythrosin B. Dry matter digestibility (DMD) values for steers given erythrosin B at a daily dosage of 6.5 mg/kg body weight were higher (P less than .05) than DMD values for control steers. DMD values were higher for steers given 16.3 or 26.1 mg erythrosin B/kg body weight daily than for the control steers, but the differences were not significant. There were no significant differences among animals given the different dosages in digestible energy. Recovery of erythrosin B from feces of treated steers varied with time, indicating that steers fed erythrosin B at a dosage of 6.5 mg/kg body weight might excrete feces during some periods of the day which would not control face fly development; however, administration of erythrosin B at a dosage of 16.3 mg/kg body weight would provide enough erythrosin B in feces to control face fly development throughout a 24-h period.     

Effect of feeding corn naturally contaminated with aflatoxin on feed efficiency, on physiologic, immunologic, and pathologic changes, and on tissue residues in steers

Two of 3 groups of Holstein-Friesian steers (groups II and III; n = 5 each) were fed a ration containing corn naturally contaminated with 800 ng of aflatoxin/g. The other group of steers (group I; n = 5) was fed a ration containing noncontaminated corn. The respective rations were fed for 17.5 weeks, except the ration given to group III; the latter's first diet (contaminated with aflatoxin) was changed to a noncontaminated diet after 15 weeks, continuing for the remaining 2.5 weeks. All steers were killed and tissues and fluids were obtained for aflatoxin analysis. Although aflatoxin B1 and M1 could be detected in blood and urine at several sampling times during the experimental period in groups II and III steers (given the diets containing aflatoxin), there appeared to be no effects on body weight gains and immune phenomena, such as lymphoblastogenesis and antibody production, but there was a waning of the delayed cutaneous hypersensitivity in steers given aflatoxin-contaminated diets. In group III animals (diet was changed to noncontaminated ration at 15 weeks), aflatoxin B1 and M1 disappeared from urine before they were slaughtered. All tissues and fluids, except the rumen contents from these group III steers, were void of detectable aflatoxins B1 and M1 at necropsy. The concentrations of aflatoxin B1 in the rumen content of the latter steers were low. All tissues collected at necropsy from the group II steers fed the aflatoxin diet throughout the 17.5 weeks had detectable aflatoxins B1 or M1 present.     

Metabolic responses to fasting and alloxan-induced diabetes mellitus in steers

To induce diabetes mellitus in 8 steers, they were fasted for 96 hours and given 110 mg of alloxan/kg of body weight (IV, in 1 dose) immediately before refeeding. Subsequently, 4 of the steers were treated with insulin (0.1 to 3 U/kg) to control hyperglycemia and 4 were not given insulin. Four control steers were fasted and refed. Fasting increased serum phosphorus, total protein, and bilirubin and decreased serum magnesium and potassium. Refeeding returned serum values of magnesium, potassium, total protein, and bilirubin toward base-line values, regardless of treatment group. However, serum phosphorus remained increased in steers with alloxan-induced diabetes and was not lowered by insulin injections. Sodium and chloride values were depressed in steers with alloxan-induced diabetes; these values remained significantly (P less than 0.05) lower than base-line values, even in steers given insulin. Fat infiltration was evident in the pancreas, liver, and to some extent, kidneys of steers with alloxan-induced diabetes, but was occasionally present in tissues of steers given insulin.     

中药组方对黄曲霉毒素B1中毒雏鸭肝功能的影响

为观察黄曲霉毒素B1(AFB1)对试验雏鸭肝功能血清指标的影响及复方中药对AFB1的颉颃效应,本试验选用7日龄健康雏鸭90只,分为3组,每组30只。Ⅰ组为空白对照组,灌胃与试验组等体积二甲基亚砜;Ⅱ组、Ⅲ组为试验组。每天分别按0.1mg/kg剂量给Ⅱ组、Ⅲ组雏鸭灌胃AFB1一次,连续投药21d,试验期间给Ⅲ组雏鸭日粮中添加2%复方中药。分别在给雏鸭投药后7、14、21d,检测雏鸭肝功能部分血清指标。结果显示,Ⅱ组、Ⅲ组雏鸭丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)与Y-谷氨酰转肽酶(GGT)活性显著高于Ⅰ组(P<0.05),而血清总蛋白(TP)与白蛋白(ALB)含量显著下降(P<0.05);与Ⅱ组比较,在日粮中添加复方中药的Ⅲ组雏鸭各项血清指标均有显著改善(P<0.05)。说明黄曲霉毒素B1导致雏鸭肝功能发生显著的变化,而复方中药能明显改善其变化。     

Acute experimentally induced aflatoxicosis in the weanling pony

Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.     

Antagonism of xylazine sedation by 4-aminopyridine and yohimbine in cattle

Twenty-four crossbred steers (4 groups of 6 steers each) were injected IM with a standard dosage range of xylazine hydrochloride (0.2 to 0.3 mg/kg of body weight). When the steers were maximally sedated, group I (control group) were given isotonic saline solution (1 ml, IV), group II were given 4-aminopyridine (4-AP, 0.3 mg/kg) IV, group III were given yohimbine hydrochloride (0.125 mg/kg) IV, and group IV were given 4-AP (0.3 mg/kg) plus yohimbine hydrochloride (0.125 mg/kg) IV. The 4-AP decreased mean standing time (MST; time until animal could stand unaided) from 94.3 minutes (control) to 13.4 minutes. Yohimbine decreased MST to 27 minutes. The combination of 4-AP + yohimbine decreased MST to 7.4 minutes. Mean total recovery time (MTRT; time from xylazine injection until normal behavior, including eating and drinking) was not significantly (P = greater than 0.05) decreased from control values by any of the antagonists tested. The combination of 4-AP + yohimbine decreased MST in animals given a 3X overdose of xylazine (0.6 mg/kg) from 124 minutes (control) to 30.3 min. The MTRT was not significantly (P greater than 0.05) decreased from control values. Two animals given a 5X overdose of xylazine (1 mg/kg) and then given 4-AP + yohimbine had a MST of 32.5 minutes and a MTRT of 3.7 hours. The combination of 4-AP + yohimbine produced marked antagonism of xylazine sedation in cattle. The combination of antagonists may prove to be useful for the arousal of animals sedated with xylazine alone or with a combination of sedatives including xylazine.     

Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.     

Effects of dietary supplementation with ethoxyquin, magnesium oxide, methionine hydroxy analog, and B vitamins on tansy ragwort (Senecio jacobaea) toxicosis in beef cattle

Dried tansy ragwort containing pyrrolizidine alkaloids was fed as 2.5% of a complete (control) diet to Hereford steers, with and without (basal) a mixture of additives. The additives provided a dietary supplement equivalent to 0.1% ethoxyquin, 1% methionine hydroxy analog, 2% MgO, 2.7 mg of vitamin B6/kg of diet, 50 micrograms of vitamin B12/kg of diet, 0.45 g of folic acid/kg of diet, and 0.2 g of cobalt/kg of diet. The additives did not alter tansy ragwort toxicity substantially, as assessed by liver histologic changes, sulfobromophthalein clearance rate, and serum gamma-glutamyl transpeptidase activity. After 281 days, 1 of 4 steers fed the basal diet was alive, whereas 3 of 4 steers in the basal plus additives group were alive, suggesting some protective activity. The chronic lethal dose of tansy ragwort in steers was 3.6% of initial body weight.     

Modification of the effects of aflatoxin B1 and warfarin in young pigs given selenium

Selenium may be related to the hepatic metabolism of the coumarin compounds aflatoxin B1 and warfarin. Selenium evidently increased the pharmacologic activity of warfarin, probably due to a displacement of warfarin from albumin by selenium, the close relationship among selenium, vitamin E, and sulphur-containing groups (eg, glutathione), or the antioxidant effect of selenium. A diet containing selenium in a concentration of 2.5 mg/kg of feed was protective against the toxic effects of both coumarins in pigs given 4 daily oral doses of 0.2 mg/kg of body weight. Selenium, as glutathione peroxidase, at least in part, protects the hepatic cells against the toxic effects of aflatoxin B1 and warfarin. The protection was demonstrated by alteration of clinical responses and hematologic (prothrombin times), electrophoretic, and clinical chemistry values. It also was demonstrated that selenium at 2.5 mg/kg of feed does not produce toxic effects; however, dietary selenium at a concentration of 5 mg/kg (and in the presence of both toxic agents) was toxic for young pigs within the 3-week experimental period. Warfarin was more active as an anticoagulant than aflatoxin B1.     

Titration of the recombinant bovine somatotropin dosage that maximizes the anabolic response in feedlot steers

The objective of this study was to determine the minimum dosage of recombinant bovine somatotropin (bST) required to elicit maximum depression in plasma urea nitrogen (PUN), an indicator of anabolic activity. Twenty-four steers (389 kg) were blocked by weight into six pens. Six steers were placed on each of the following bST doses: 0, 8, 16 and 32 mg bST/d. Treatments were administered once daily via subcutaneous injections for 21 d. Steers were weighed and jugular blood samples were taken on d 0, 1, 4, 7, 10, 13, 16 and 21 at 1400, approximately 4 h after feeding. Delta PUN (DPUN) was calculated as PUN - d 0 PUN. There was no dose x time interaction (P = .94) in DPUN. Maximum reduction in DPUN with bST occurred by d 7 (P less than .05). Linear (P less than .01) and quadratic (P less than .05) orthogonal contrasts indicated that DPUN depression increased with bST administration, with maximal reduction calculated to occur with 23 mg (59 micrograms/kg) bST/d. There was no further decrease in DPUN with 32 than with 16 mg bST, indicating that the minimum daily dose is at least 16 mg but no more than 23 mg. A similar dose response was observed in daily gain. Results from this study indicate that bST reduced PUN in a dose-dependent manner and that 41 to 64 micrograms/kg body weight maximized the anabolic effect of bST in growing steers.     

Alteration of neutrophil function associated with coccidiosis in cattle: influence of decoquinate and dexamethasone

Twenty Holstein steers subclinically infected with coccidia were allotted to 2 groups of 10 steers each. One group received a diet containing 0.5 mg of decoquinate/kg of body weight. After 25 days on the diet, there was no difference between the groups in lymphocyte blastogenic responsiveness to mitogens; however, there were differences in neutrophil function. Lymphocytes from steers of the decoquinate-fed group had decreased random migration under agarose, enhanced cytochrome C reduction, and enhanced iodination activity. Other measures of neutrophil function evaluated (chemotactic index, Staphylococcus aureus ingestion, and antibody-dependent and -independent cell-mediated cytotoxicity) were not affected. After 30 days of decoquinate feeding, half of the cattle in each group received 5 daily IM injections of dexamethasone (0.04 mg/kg of body weight). The dexamethasone-treated steers from the group that did not have decoquinate in the diet developed clinical coccidiosis, whereas the decoquinate-treated steers remained clinically normal. Lymphocyte and neutrophil function were again evaluated for a 3-day period beginning 4 days after dexamethasone treatment was halted. Neutrophils from the steers that developed clinical coccidiosis after dexamethasone administration had significantly (P less than 0.05) inhibited random migration under agarose, cytochrome C reduction, and iodination activity, but significantly (P less than 0.01) enhanced S aureus ingestion. The feeding of decoquinate prevented the inhibition of neutrophil cytochrome C reduction and lessened the inhibition of neutrophil iodination in the dexamethasone-treated group. Dexamethasone treatment was associated with an inhibition of lymphocyte blastogenic responsiveness to phytohemagglutinin in principals as well as controls.     

Changes in plasma concentrations of thyroxine and triiodothyronine in beef steers fed different levels of propylthiouracil

Three Latin-square trials were conducted to determine the effects of feeding the thyroid depressant propylthiouracil (PTU) on plasma concentrations of thyroxine (T4) and triiodothyronine (T3) in feedlot steers. In trial 1, four steers were fed 0, 1, 2 or 4 mg PTU/kg body weight daily during five 35-d experimental periods. In trial 2, eight steers were fed 0, .5, 1 or 2 mg PTU/kg body weight daily during five 28-d periods. In trial 3, three steers were fed 0, 1 or 4 mg PTU/kg body weight daily during the first 3 d in each of three 28-d periods. In general, feeding PTU caused increases in plasma T4 concentrations that peaked 5 to 7 d after feeding started. Concurrently, T3 concentrations tended to decrease when PTU was fed. The effects of PTU on hormone concentrations were apparent within approximately 1 to 4 h after PTU feeding started. Furthermore, when PTU was not fed, T4 and T3 concentrations appeared to have rhythmic cycles of 90 and 111 min, respectively, and PTU treatment appeared to interrupt this cyclical pattern. After the initial PTU response, the dose response relationship between PTU level and plasma hormone concentration was not linear. Both 4 and 2 mg PTU appeared to depress both T4 and T3 concentrations, suggesting direct inhibition of the thyroid gland and, for the 1-mg PTU treatment, T4 tended to stabilize at concentrations significantly greater than for 0 mg PTU, while T3 concentrations for 1 mg PTU were slightly lower than for 0 mg PTU.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute aflatoxicosis in swine: clinical pathology, histopathology, and electron microscopy

Feeder pigs weighing 12 to 15 kg each were given a single oral dose of aflatoxin, 1.2 mg/kg of body weight. Liver-specific serum enzyme activities were compared with gross, microscopic, and ultrastructural hepatic changes in individual pigs euthanatized at 24, 48, and 72 hours after they were given aflatoxin. The greater the morphologic change in liver of the treated pigs, the greater the increase in liver-specific serum enzyme activities. Isocitric dehydrogenase, alkaline phosphatase, sorbitol dehydrogenase, and aspartate aminotransferase activities increased in 6 of 8 treated pigs by 24 hours. Increase in gamma-glutamyl transpeptidase activity was not significant. Microscopic and ultrastructural changes in centrilobular hepatocytes included glycogen deletion, mitochondrial and endoplasmic reticulum swelling, membrane disruption, and nuclear fragmentation at 24 hours. The centrilobular areas had marked extravasation of erythrocytes at 24 hours without basal lamina changes. At 72 hours, the centrilobular hepatocytes had increased lipid vacuoles and acceptable amounts of glycogen. Marked infiltrations of monocytes, plasma cells, and lymphocytes were also present at this time.     

Lasalocid toxicity in cattle: acute clinicopathological changes

Thirty-six steers (148 to 500 kg) divided into six equal groups were used in a toxic syndrome study of lasalocid and monensin given as a single oral dose. One group was given a placebo, a second group received monensin (25 mg/kg body weight) and the other four groups received lasalocid at 1, 10, 50 or 100 mg/kg body weight (bw). No toxic signs developed in cattle given placebo or lasalocid at 1 or 10 mg/kg bw dose. The earliest toxic signs were muscle tremors, tachycardia and rumen atony. After 24 h, the cattle were dehydrated, anorectic and had diarrhea. Deaths occurred between d 1 and 22.5 in the groups receiving lasalocid at 50 and 100 mg/kg bw and monensin. Altered values in blood leucocytes, erythrocytes, hemoglobin, hematocrit, total protein, albumin, creatinine, urea nitrogen, total bilirubin, creatine kinase, lactic dehydrogenase, calcium, chloride and inorganic phosphate occurred 1 d after dosing: urine pH and specific gravity also changed 1 d after dosing. Maximum changes occurred at d 3. Most of the changes were indicative of dehydration rather than specific organ damage.     

Effects of aflatoxin M1 intake at physiologic levels on newborn dairy calves

When aflatoxin-contaminated grain is consumed by dairy cows, aflatoxin M1 is excreted in the milk. Sixteen neonatal male Holstein calves were given milk which had been collected from cows given 5 to 6 mg of aflatoxin B1 each day. The calves were examined for possible detrimental effects of the mycotoxin at pseudophysiologic concentrations. Calves were allotted to 1 of 4 groups given different milk dietary aflatoxin M1 concentrations: group 1--given 0 microgram of aflatoxin M1/L (undetectable); group 2--given 0.5 microgram/L; group 3--given 1 microgram/L; and group 4--given 2 micrograms/L. Whole milk equal to 8% of body weight was fed daily and adjusted each week to maintain this ratio. Water and a 15% crude protein complete calf starter ration were offered ad libitum for the 6-week feeding study. Weekly blood samples were collected via jugular venipuncture and analyzed for serum alkaline phosphatase and aspartate aminotransferase activities. Daily means for milk dry matter intake (in kg) and complete ration intake (in kg) for the calf groups were as follows: 0.46 and 0.36 for group 1; 0.46 and 0.25 for group 2; 0.42 and 0.18 for group 3; and 0.49 and 0.40 for group 4. Significant differences in complete ration and total dry matter intake were noted. The average daily gains (in kg) and gains in height at withers (in cm) were 0.39 and 4.1 for group 1; 0.36 and 4.0 for group 2; 0.29 and 5.7 for group 3; and 0.42 and 5.1 for group 4.(ABSTRACT TRUNCATED AT 250 WORDS)     

Depletion of intramuscularly and subcutaneously injected procaine penicillin G from tissues and plasma of yearling beef steers.

Withdrawal periods required when doses of 24,000 IU and 66,000 IU of procaine penicillin G/kg body weight were administered to yearling beef steers by intramuscular injection daily for five consecutive days were investigated. These dosages are in excess of product label recommendations, but are in the range of procaine penicillin G dosages that have been administered for the treatment of some feedlot bacterial diseases. The approved dose in Canada is 7,500 IU/kg body weight intramuscularly, once daily, with a withdrawal period of five days. Based on the tissue residue data from this study, the appropriate withdrawal period is ten days for the 24,000 IU/kg body weight dose and 21 days for the 66,000 IU/kg body weight dose when administered intramuscularly to yearling beef steers. In a related study, 18 yearling beef steers received 66,000 IU of procaine penicillin G/kg body weight administered by subcutaneous injection, an extra-label treatment in terms of both dose and route of administration, typical of current practice in some circumstances. Deposits of the drug were visible at subcutaneous injection sites up to ten days after injection, with more inflammation and hemorrhage observed than for intramuscular injections of the same dose. These results suggest that procaine penicillin G should not be administered subcutaneously at high doses; and therefore a withdrawal period was not established for subcutaneous injection.     

Toxicologic evaluation of chlorpyrifos in cats

Twenty-four male domestic shorthair cats were used to evaluate the acute and chronic effects of a single, toxic but sublethal, orally administered dose of chlorpyrifos. A dosage of 10 mg/kg of body weight did not induce clinical signs of toxicosis, but a dosage of 40 mg/kg induced clinical signs of toxicosis, and 1 of 12 cats died. Chlorpyrifos given at a dosage of 0.1 mg/kg to 2 cats reduced whole blood and plasma cholinesterase (Che) activities to values obtained after cats were given doses that induced clinical signs of toxicosis. Regeneration time for whole blood and plasma Che activities ranged from 7 to 28 days. Brain Che activity was considerably decreased in 1 cat that died 4.5 hours after dosing, but was normal in all others at 28 days after dosing. Other than decreased Che activity, significant changes were not seen in hematologic or serum biochemical values. Toxin-related lesions were not seen during macroscopic or microscopic examination.     

The effect of high doses of aflatoxin on the pig]

In two experiments, 18 pigs were given feed contaminated with aflatoxin which had been prepared by the extraction of the cultures of toxinogenic strains of the fungus Aspergillus flavus. After the ingestion of aflatoxin (AFB1) at a dose of 5.4 to 10.5 mg per kg of live weight, the pigs showed symptoms of peracute aflatoxicosis and died within 12--20 hours. After ingestion of AFB1 at a dose of 1.4 or 3.1 mg per kg live weight, the pigs suffered from acute aflatoxicosis and died within 3 to 26 days from the administration of the contaminated feed. In the cases of these experimental aflatoxicoses, clinical symptoms, haematological and biochemical changes in the blood and the patho-anatomical and histological findings in the swine organism were described.