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

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

Behavioral, nutritional, and toxicological responses of cattle to ensiled leafy spurge.

Yearling cattle (n = 25; 416.1 +/- 25.9 kg) were stratified by weight and gender across five groups. Group 1 (OAT) was offered oat/rape haylage (ORH) for ad libitum consumption during two daily feeding periods. Group 2 (SPURGE) was offered leafy spurge/grass haylage (LSGH) for ad libitum consumption during the same feeding periods. Group 3 was offered ORH in an amount equal to the average amount of LSGH consumed by SPURGE at the previous feeding. Group 4 (MIX) was offered LSGH mixed with ORH for ad libitum consumption during the two feeding periods. Group 5 (PAIR) received the equivalent amount of ORH consumed by MIX at the previous feeding. The DMI for OAT, SPURGE, and MIX were similar at the first feeding (P = .52). The SPURGE group consumed very little LSGH thereafter and was removed from the trial. The OAT and MIX groups consumed similar amounts of DM daily on d 1 to 4 when the ration offered to MIX was only 7% LSGH (P = .33). When LSGH made up > or = 21% of the mixture (d 7 to 32), the OAT group consumed more daily DM than did MIX (P < .05). The spurge/oatlage ration offered to MIX was less digestible than the oatlage-only ration offered to PAIR (P < or = .01). Even though blood chemistry did not indicate that LSGH consumption caused organ damage, its intake caused minor alterations (P < or = .05) in serum albumin, calcium, gamma glutamyltransferase, P, K, and urea nitrogen. No gross or microscopic lesions, infectious agents, or significant numbers of parasites were detected in any of the carcasses or tissues examined. The MIX group had diarrhea for much of the trial. In Trial 2, five yearling cattle were adapted to a mixture of 21% LSGH and 79% ORH. Then they were simultaneously offered three mixtures of spurge and oat haylages: 1) spurge ensiled with a microbial inoculant (LSGH); 2) spurge ensiled with the same inoculant and a cellulolytic/hemicellulolytic enzyme (ENZ); and 3) spurge ensiled with the same inoculant and molasses (MOL). The mixture with ENZ was preferred over those with MOL or LSGH (P < .001), but the amounts consumed were low and similar to those for LSGH-ORH in Trial 1 when amounts of ENZ and LSGH in the mixtures were similar. The ENZ mixture may have been more palatable than LSGH and MOL because it had less (P < .05) lactic acid, but intake of ENZ indicates that it had aversive characteristics, like LSGH. Ensiling leafy spurge did little, if anything, to improve its palatability to cattle.

The effect of subclinical selenium toxicosis on pregnant beef cattle.

A field investigation conducted by the South Dakota Animal Disease Research and Diagnostic Laboratory suggested that subclinical selenium toxicosis in pregnant cows may have contributed to an outbreak of aborted/stillborn calves in a high-selenium region of South Dakota. This study was undertaken to evaluate the relationship between abortion and subclinical selenium toxicosis in the dam and to assess the effects of subclinical selenium toxicosis on the bovine immune system. Fifteen pregnant cows were fed diets containing 0.25 (control), 6.0, and 12.0 ppm selenium beginning at 80-110 days gestation. Although selenium toxicosis has been reported to cause abortion, this study failed to reproduce abortions. A single cow in the 12-ppm selenium treatment group gave birth to a weak calf, which subsequently died. This calf had myocardial lesions consistent with those described for selenium toxicosis and had hepatic selenium levels of 9.68 ppm (wet weight). Elevated dietary selenium resulted in the depression of several leukocyte function parameters in pregnant cows. A statistically significant depression in forced antibody response was identified in both selenium-supplemented groups. A significantly diminished mitogenic response to concanavalin A and pokeweed mitogen was also observed in the 12-ppm selenium group. Although a similar pattern of depression was also observed with phytohemagglutinin, differences were not significant. These findings indicate that even in the absence of clinical alkali disease, elevated selenium levels may adversely affect both pregnancy outcome and the bovine immune system.

The short-term effect of low concentrations of dietary aflatoxin and T-2 toxin on mallard ducklings.

Two 9-day trials to study effects of dietary mycotoxins were conducted using 6-week-old mallards. Each trial involved three groups of six ducks each, three males and three females per group. One group was fed no myocotoxin (control), one was fed aflatoxin, and the third was fed T-2 toxin. Dietary aflatoxin was 12 ppb in trial 1 and 33 ppb in trial 2; dietary T-2 toxin was 2 ppm in both trials. There were no gross or microscopic lesions in controls or in ducks fed aflatoxin, nor did these groups differ significantly in final body weight or in weights of spleen or bursa of Fabricius. Ducks exposed to T-2 toxin had erosions and/or ulcerations in the oral cavity and esophagus; further, these ducks exhibited a decrease in weights of body, thymus, spleen, and bursa of Fabricius. The only microscopic change seen in lymphoid organs of ducks exposed to T-2 toxin was a moderate decrease of thymic cortical lymphocytes.

Confirmation of indandione rodenticide toxicoses by mass spectrometry/mass spectrometry.

Mass spectrometry/mass spectrometry (MS/MS) with collision-activated dissociation (CAD) was utilized to unequivocally distinguish 1,3-indandione rodenticides in 2 cases of anticoagulant toxicosis. Anecdotal evidence provided by the veterinarian in a case involving feedlot cows and physical evidence at the site of occurrence in a similar case involving lambs strongly implicated diphenadione (diphacinone; DP) in both instances. However, high performance liquid chromatography indicated chlorophacinone (CP), not DP, was present in the blood samples obtained from both cows and lambs. Intact 1,3-indandiones exhibit poor gas chromatographic properties, so procedures were developed for analysis by MS/MS using a direct exposure probe for sample introduction. The EI mass spectra of DP and CP contained a base peak at m/z 173, with molecular ions (M+) at m/z 340 and m/z 374 (Cl isotope cluster), respectively. Corresponding MS/MS CAD parent ion spectra of m/z 173 showed an ion of m/z 340 for DP and 374 (Cl cluster) for CP. CAD analysis of the blood extracts showed a parent ion scan of m/z 173 identical to that of CP, with the m/z 374 (Cl cluster). (Additional evidence was obtained by MS/MS examination of the CAD daughter ion spectrum of m/z 374.) Blood extracts from the affected animals revealed CAD daughter ion spectra for m/z 374 identical to that of reference CP. Positive confirmation of CP in both cases led to identification of the source of the toxicant and prevention of further animal exposures.

Arsenic concentrations in tissues and body fluids of dogs on chronic low-level dietary sodium arsenite.

Twenty-four female Beagle dogs, 7-8 months old, were assigned to 4 groups. Control, low-dosage, medium-dosage, and high-dosage groups were offered 0, 1, 2, and 4 mg of sodium arsenite per kilogram of body weight per day (mg/kg/day), respectively, in their feed (equivalent to 0.0, 33.4, 66.7, and 133.4 micrograms/g in feed). On day 59, the dosage was doubled for the rest of the experiment, which ended on day 183. In general, arsenic concentrations in tissues and body fluids reflected arsenic levels in feed. Arsenic caused a dose-related decrease in food intake. Statistically significant differences in blood, liver, and kidney arsenic were detected, in most cases, between the 2 higher dosage groups and controls. The greatest differences in arsenic concentrations between groups were present in urine and hair. Results indicate that urine and hair would be the most useful specimens for chemical analysis when attempting to confirm low-level dietary inorganic arsenic exposure or poisoning.

Attaching and effacing Escherichia coli infection as a cause of diarrhea in young calves.

A form of enteric Escherichia coli infection was identified in 60 calves from 59 farming operations. The E coli responsible for these infections principally colonized the colon, inducing a distinctive lesion described as attaching and effacing. Hemorrhagic enterocolitis or blood in the feces was observed on 40% of the farms. Of affected calves, 86.6% were dairy calves (average age, 11.8 days). Forty-four calves were infected concurrently with other enteropathogens (cryptosporidia, rotavirus, coronavirus, enterotoxigenic E coli, bovine viral diarrhea virus, coccidia). Verotoxin-producing E coli was recovered from 31 calves; 8 were serotype O111:NM isolates, 3 were serotype O5:NM, and 1 was serotype O26:NM.

Effect of subacute low level dietary sodium arsenite on dogs.

Thirty female beagle dogs, 7 to 8 months old, were assigned to five groups. Control, low dosage, medium dosage, high dosage, and pair-fed groups were offered 0, 1, 2, 4 and 0 mg of sodium arsenite per killigram of body weight per day (mg/kg/day), respectively, in their feed. On Day 59, the dosage was doubled for the rest of the experiment, which ended on Day 183. Nominal dosages of 4 and 8 mg/kg/day caused a significant decrease in feed consumption. The initial decreased feed consumption was followed by increased intake over time. Nominal dosages of 4 and 8 mg/kg/day caused a significant decrease in body weight. Body weight loss of high dosage and pair fed groups were not significantly different. Serum aspartate aminotransferase was elevated in dogs exposed to 4 and 8 mg/kg/day of sodium arsenite. Serum alanine aminotransferase was elevated in dogs exposed to 2, 4, and 8 mg/kg/day. No gross or light microscopic lesions were present in the liver of any group. This study shows that dietary sodium arsenite causes a dose-dependent decrease of feed consumption and body weight. Weight loss is caused by decreased feed consumption, not by the direct effect of the sodium arsenite.

Renal percent clearance ratios in cattle.

Renal percent clearance ratios for various electrolytes were determined on nine clinically normal Holstein heifers. Endogenous creatinine serum and urine levels were used to calculate the ratios. The average percent clearance ratios and standard deviations of Na, K, Cl, P, and Ca were 1.97+/-0.63, 49.3+/-9.2, 3.16+/-1.l2, 15.6+/-14.3, and 1.38+/-1.41, respectively. The correlation between Na and Cl percent clearance ratios within a sample was 0.92. A very strong direct correlation of urine creatinine and urine specific gravity was demonstrated.