The effect of feeding monensin, with or without dry hay plus wilted forage, on ruminal formation of 3-methylindole (3MI) was investigated in pastured cattle. Eighty-two cows were allotted to 3 groups. Cows of group-1 served as controls and were given a daily energy supplement (1 kg/head) without monensin for 1 day before and for 7 days after being allowed access to lush pasture. Cows of groups 2 and 3 were given the same daily energy supplement, which also contained monensin (200 mg/kg of supplement). Cows of group 3 also were fed dry hay for 5 days before the start of the study and continued to be given supplemental hay for 4 days after being allowed access to lush pasture containing a layer of wilted forage. Ruminal 3MI and indole concentrations increased on day 1 after all groups were allowed access to lush pasture. By day 7, 3MI concentration in all cows had decreased to pregrazing concentration. Indole concentration did not reach pregrazing concentration until day 10 for cows of groups 1 and 2. Group-3 cows had pregrazing indole concentration on day 7. Ruminal indole concentration did not differ (P > 0.05) between groups 1 and 2. Ruminal indole concentration was lower (P < 0.01) in group-3 cows on all sample collection days, except day 10, compared with that in the other groups. Monensin reduced (P < 0.01) 3MI formation on days 1 and 7 in group-2 cows, compared with group-1 cows. Group-3 cows had lower 3MI concentration than did group-1 cows (P < 0.01) on days -1, 1, 4, and 7. Monensin, when fed with dry hay and wilted forage, reduced (P < 0.01) 3MI formation on days 4 and 7 in group-3 cows, compared with cows that were only given monensin (group 2). Group-3 cows also had lower (P < 0.05) 3MI concentration, compared with group-2 cows on day 1. Results indicated that monensin reduced ruminal formation of 3MI. Feeding dry hay and wilted forage to cattle during the change to lush pasture resulted in further reduction in the amount of 3MI formed by ruminal microorganisms. To maximize the effectiveness of monensin in reducing 3MI formation, dry hay plus wilted forage should be fed to pastured cattle for at least 4 days after they are allowed access to lush pasture.

The hematologic and pathologic effects of orally administered L-tryptophan and indoleactic acid and of L-tryptophan administered IV were studied in ponies. Sixteen adult Shetland ponies were allotted into 4 experimental groups. Group 1 consisted of 5 ponies (1-5) given 0.6 g of tryptophan/kg of body weight in a water slurry via stomach tube. Group 2 included 4 ponies (6-9) given 0.35 g of tryptophan/kg orally. Group-3 ponies (10-13) were given 0.35 g of indoleacetic acid/kg orally. Group 4 consisted of 3 ponies (14-16) given a single 4-hour IV infusion of 0.1 g of tryptophan/kg. Restlessness, increased respiratory rate, hemolysis, and hemoglobinuria were detected in 4 of the 5 group-1 ponies. Only pony 7 in group 2 developed hemolysis, hemoglobinuria, and a significant increase in respiratory rate. Renal pathologic lesions, consistent with hemoglobinuric nephrosis, were seen in ponies 2, 4, 5, and 7. Bronchiolar degeneration was evident in 4 of 9 ponies given tryptophan orally. The importance of these respiratory lesions was unknown. Clinical or pathologic abnormalities were not noticed in the ponies of groups 3 and 4. Mean plasma tryptophan values increased significantly in groups 1 and 2 at 6 hours after dosing. A second peak of tryptophan was detected in both groups at 12 hours. Values returned to predose values by 48 hours. Plasma indole and 3-methylindole concentrations were detectable in only 2 ponies (4 and 7). In vitro incubations of cecal fluid from ponies 6, 8, and 9 yielded a percentage conversion of tryptophan to indole of 16.75%, 5.84%, and 7.96%, respectively. 3-Methylindole was not produced. These results suggested that indole was the major metabolite of orally administered tryptophan in these ponies.

An in vitro bioassay system was used to study the effects of cyclopiazonic acid (CPA) mycotoxin on cardiac muscle. Acute exposure to 6 microgram of CPA/ml of modified Krebs-Henseleit solution significantly (P < 0.05) decreased 5 in vitro turkey cardiac muscle performance criteria: maximal weight a muscle could lift; maximal contraction velocity; relaxation velocity; time to peak contraction; and total time for muscle contraction and relaxation. The effect on these 5 criteria appeared to result from intracellular changes partially associated with calcium availability and were irreversible, suggesting that physiologic changes had developed after acute exposure to CPA.

The aim of this study was to evaluate the occurrence of Shiga toxin (stx)-producing Escherichia coli (STEC) in diarrheic newborn calves, as well as the resistance profile of this microorganism against antimicrobials routinely used in veterinary therapy. The antimicrobial profile of Eugenia uniflora against E. coli clinical isolates was also analyzed. Specimens from the recto-anal junction mucosa were investigated by using chromogenic medium and identification of E. coli was done using microbiological methods (Gram staining, indole test, methyl red test, Voges-Proskauer test, citrate test, urease test, and hydrogen sulfide test). The stx1 and stx2 genes corresponding to the STEC pathotype were evaluated by using polymerase chain reaction and electrophoresis. The susceptibility profile to antimicrobial agents commonly used in veterinary therapeutic practice and the antimicrobial effect of lyophilized hydroalcoholic extract of E. uniflora L. leaves against E. coli clinical isolates were evaluated by disk diffusion and microdilution methods. Shiga toxin-positive E. coli was identified in 45% of diarrheic newborn calves (stx1 = 23.2%, stx2 = 4.0%, stx1 + stx2 = 18.2%). The frequency of stx-positive E. coli in the bacterial population was equal to 17.0% (168/990 clinical isolates): 97 (9.8%) stx1-positive E. coli, 12 (1.2%) stx2-positive E. coli, and 59 (6.0%) stx1 + stx2-positive E. coli isolates. All stx-positive E. coli analyzed showed resistance to multiple drugs, that is, from 4 to 10 antimicrobials per clinical isolate (streptomycin, tetracycline, cephalothin, ampicillin, sulfamethoxazole + trimethoprim, nitrofurantoin and nalidixic acid, ciprofloxacin, gentamicin, and chloramphenicol). Effective management measures should be implemented, including clinical and laboratory monitoring, in order to promote animal and worker health and welfare, prevent and control the spread of diseases, and ensure effective treatment of infectious diseases. The E. uniflora L. leaves showed inhibition of microbial growth based on the diameter of halos, ranging from 7.9 to 8.0 mm and 9.9 to 10.1 mm for concentrations of 50 and 150 mg/mL, respectively. This plant displayed bacteriostatic action and a minimum inhibitory concentration of 12.5 mg/mL for all clinical isolates. Its clinical or synergistic effects with antimicrobial agents must be determined from clinical and preclinical trials.

Eight ponies were allotted to 2 groups of 4. Group-1 ponies (1-4) were given 0.2 g of indole/kg of body weight orally and group-2 ponies (5 to 8) were given 0.1 g of indole/kg. Various physical, hematologic, and physiologic measurements were obtained after administration of indole. Intravascular hemolysis and hemoglobinuria were detected in both groups within 24 hours of dosing. Hemolysis was reflected by decreases in PCV, hemoglobin concentration, and RBC count, and an increase in indirect bilirubin. Erythrocyte fragility appeared to increase in both groups at 8 hours after dosing and peaked at 16 hours after dosing. At 72 hours after dosing, the RBC fragility value was less than predose measurements. Heinz body formation was noticed in group-2 ponies, but not in group 1. Plasma indole concentrations increased in both groups from the nondetectable predose concentrations. Group-1 values were 203% of group-2 values. In group 2, plasma indole was nondetectable by 12 hours, whereas low concentrations could still be measured in the group-1 ponies at 24 hours. Ponies in group 1 died or were euthanatized between 24 and 72 hours after dosing, whereas group-2 ponies were euthanatized between 48 and 120 hours. At necropsy, all body fat, mucous membranes, and elastic tissue were stained yellow. Hemoglobinuric nephrosis was the most prominent microscopic lesion. Results of this study indicated that indole, a metabolite of the amino acid tryptophan, causes acute intravascular hemolysis in ponies.