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W B Buck

Publications and source records attributed to W B Buck.

At least 37 records · Page 2Linked to original sources
PubMed1992

Case reports of lead poisoning in dogs from the National Animal Poison Control Center and the Centre National D'Informations Toxicologiques, Veterinaires: anecdotes or reality?

This paper presents case reports of lead toxicoses from 2 major animal poison control centers in Europe and North America, gathered from 1985 through 1989. All results examined here involved cases assessed as "toxicosis" or "suspected toxicosis" by the National Animal Poison Control Center (NAPCC) or the Centre National d'Informations Toxicologiques Veterinaries (CNITV). 537 cases were reported to the NAPCC, most of them concerning dogs (59%). In France, most of the 362 cases involved cattle (57.2%). There was an increased number of cases reported during late summer and early fall, and a decreased number of cases in November and December, in both centers. Dogs intoxicated were predominantly young animals (60% were less than 2 years old). No sex difference was noted. Pure bred dogs appeared more often involved than mixed-breed ones, but the breed distribution closely resembles dog breed distribution in the US. The source of lead was usually unknown and, when information was available, paint seemed to be the most common cause of poisoning. Clinical signs reported to the animal poison control centers involved the CNS and GI tract. Results from the French and the American database showed similar trends. They are compared to data from veterinary clinics and veterinary colleges in the US and Australia. In each case, data are very similar to what was reported to the CNITV and the NAPCC. It is concluded that animal poison control centers databases can provide a useful tool for better knowledge of animal poisoning. They can also help identify unexpected toxicologic problems related to drug administration or pesticide use.

Age Factors↗
PubMed1991

Regional brain blood flow in swine following T-2 toxin administration.

Three groups of swine (6/group) were used to assess alterations in regional brain blood flow induced by T-2 toxin. One group served as vehicle (70% ethanol) control, and groups were dosed intravascularly with T-2 toxin at 0.6 or 2.4 mg/kg body weight. Cerebral, cerebellar, and brain stem blood flows were evaluated at 0 h (predosing) and at 90-min intervals for 6 h postdosing. Fifteen-micron diameter radionuclide labeled microspheres were used to determine blood flow. Hemodynamic variables were determined at the same time points. The infusion of T-2 toxin resulted in dose-dependent reductions in both cardiac index and mean arterial pressure, accompanied by significant increases in heart rate. In animals given the lower dose of T-2 toxin, significant reductions in blood flow were evident in the cerebrums and cerebellum but not in the brain stem. Reductions in blood flow to all regions of the brain were evident in those animals given 2.4 mg T-2 toxin/kg. Brain blood flow was less severely compromised than was cardiac output, suggesting intact local autoregulation.

Animals↗
PubMed1991

Electroencephalographic changes associated with bromethalin toxicosis in the dog.

Electroencephalogram (EEG) recordings were obtained before and during the clinical syndrome induced by a bromethalin rodenticide given to dogs. Nine dogs given 6.25 mg bromethalin/kg po developed clinical signs and EEG abnormalities 15 to 58 h postdosing. Predominant abnormal EEG changes included spike and spike-and-wave EEG patterns (66%), high voltage slow wave (HVSA, 50-150 microV, 1-6 Hz) activity (44%) photoconvulsive or photoparoxysmal irritative responses (44%), and marked voltage depression (dominant activity less than 10 microV) in all leads (33%).

Aniline Compounds↗
PubMed1990

Fenvalerate/N,N-diethyl-m-toluamide (Deet) toxicosis in two cats.

Toxicosis attributable to fenvalerate and N,N-diethyl-m-toluamide (Deet) exposure was suspected in 2 cats. Clinical signs of toxicosis developed within 4 to 6 hours of dermal application of the pesticide. Clinical signs of toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition, seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and brain tissues confirmed the presence of fenvalerate and Deet. The pyrethroid fenvalerate and the insect repellent Deet are used for the control of fleas and ticks on cats. Suspected fenvalerate/Deet toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting, depression, and seizures.

Animals↗
PubMed1990

Prevention of T-2 toxin-induced morphologic effects in the rat by highly activated charcoal.

The efficacy of a highly activated charcoal in preventing the morphologic effects of T-2 toxin was examined in female rats. T-2 toxin at 25 mg/kg (6 x LD50) was given orally to all rats. Half the rats also received the charcoal, at a dose of 9 ml/kg and a concentration of 104 mg/ml, while the other half received water. A charcoal-treated rat (T-2 toxin + charcoal) was killed at the time of death of each positive control animal (T-2 toxin alone). Severe necrosis was seen in the spleen, thymus, stomach, small intestine, liver and adrenal glands of the positive controls (T-2 toxin alone). Lesions were absent or minimal in the paired charcoal-treated rats (T-2 toxin + charcoal).

Adrenal Cortex↗
PubMed1990

Diagnosis of bromethalin toxicosis in the dog.

Dogs given a single oral dose of bromethalin at 6.25 mg/kg developed a toxic syndrome characterized by hyperexcitability, tremors, seizures, depression, and death within 15-63 hours after bromethalin administration. Gross lesions included mild cerebral edema (2/5) and mild pulmonary congestion (2/5). Histologic lesions included diffuse white matter spongiosis (5/5), mild microgliosis (3/5), optic nerve vacuolization (3/5), mild thickening of Bowman's capsule (2/5), and occasional splenic megakaryocytes (2/5). Ultramicroscopic examination of midbrain stem revealed occasional swollen axons, intramyelinic vacuolization, and myelin splitting at the intraperiod line. Bromethalin was detected in kidney, liver, fat, and brain tissues, using gas chromatography with electron capture detection. Photodegradation of extracted bromethalin may limit accurate quantification of tissue residues.

Adipose Tissue↗
PubMed1989

Acute aflatoxicosis in feeder pigs, resulting from improper storage of corn.

Aflatoxicosis was diagnosed in 600 feeder pigs, of which 400 died, 150 were destroyed, and 50 were marketed. The pigs were exposed to 2,500 to 3,500 micrograms of aflatoxins/kg of feed. Drought-stressed damaged corn infected with Aspergillus flavus was stored under ambient conditions in a glass-lined silo, and this storage environment provided conditions that favored rapid fungal growth and mycotoxin production.

Aflatoxins↗
PubMed1989

Cottonseed meal (gossypol) toxicosis in a swine herd.

Cottonseed meal (CSM) that contained a high concentration of free gossypol was inadvertently used as a protein supplement, without appropriate iron supplementation, for a swine herd in Illinois. Fifty percent of 300 grower and finishing swine died, and an additional 20% became ill during a 4- to 6-week period. Clinical signs included respiratory distress and abdominal distention. At necropsy, the hearts were diffusely pale, flaccid, and rounded because of dilatation of all 4 chambers, the livers were large and congested, and hydropericardium, hydrothorax, and ascites were evident. Histologic changes consisted of diffuse myocardial fiber atropy with perinuclear vacuolation, and multifocal myocardial and skeletal muscle necrosis. Changes in the liver included marked centrilobular congestion, loss of hepatocytes, and fatty degeneration. Differential diagnoses included monensin, selenium, and gossypol toxicoses, and vitamin E/selenium deficiency. Analyzed feed samples did not contain monensin. Feed selenium concentrations ranged from 428 to 1,513 micrograms/kg, and iron concentrations from 160 to 180 mg/kg. Cottonseed meal (3 to 10%) was detected by feed microscopy. A sample of the 40% protein supplement contained 19% CSM and 1,300 mg of free gossypol/kg, whereas feed samples contained 200 to 400 mg of free gossypol/kg. The history, clinical signs, pathologic findings, and feed analyses were compatible with a diagnosis of gossypol toxicosis. Cottonseed meal, a high-protein supplement used widely in southern United States, may contain gossypol (a polyphenolic binaphthalene pigment), which in its free form is especially toxic to simple-stomached animals. If CSM is used, supplementation with ferrous sulfate is recommended at a 1:1 weight ratio with free gossypol, up to 400 mg of FeSO4/kg.

Animal Feed↗
PubMed1989

Dinoseb toxicosis in two dogs.

Two male English Setters were noticed to be breathing rapidly, hyperexcitable, and atactic after roaming a rural area for 2 hours. Both dogs' cost were stained with yellow liquid. One dog died while en route to the veterinarian. Treatment was begun for the surviving dog for what was initially diagnosed to be organophosphorus or carbamate insecticide toxicosis. Before the diagnosis could be confirmed, the second dog died. The yellow liquid on the dogs' skin was identified as dinoseb in high concentrations. Dinoseb is an acutely toxic, substituted dinitrophenolic herbicide believed to act as an uncoupler of electron transport from oxidative phosphorylation.

2,4-Dinitrophenol↗
PubMed1989

Evaluation of a superactivated charcoal paste and detergent and water in prevention of T-2 toxin-induced local cutaneous effects in topically exposed swine.

T-2 toxin (6 mg) dissolved in 90% DMSO was topically applied to nine 9-cm2 sites on the dorsum of each of nine young, crossbred, specific pathogen-free, female pigs, 20.6 +/- 1.9 kg in weight. A superactive charcoal paste (SAC) and/or a soap-and-water wash (SOAP) was applied to eight of the T-2-exposed sites on each animal. These treatments were applied at various times postexposure ranging from 5 to 65 min. The site that received T-2 alone served as a positive control. DMSO was applied to a tenth site on each pig as a negative control. Animals were killed 1, 3, or 6 days after treatment. Skin lesions were examined and graded grossly and histologically. No adverse systemic clinical signs were observed in any of the animals. Marked reddening and slight swelling of the T-2 toxin-treated positive control sites were present throughout the study. Ulceration of this site was first noted on Day 3. All therapeutic regimens effectively reduced lesion severity resulting from T-2 toxin application. Significant differences in relative effectiveness were also seen between treatments. In each significant pair, the ordering of mean lesion severity was SAC/SOAP less than SAC or SOAP and SOAP less than SAC. As a single treatment, SOAP appears to be more effective than SAC in reducing lesion severity. These results failed to provide unequivocal evidence of an additive therapeutic effect when SAC and SOAP were used sequentially on the same site.

Administration, Topical↗
PubMed1989

Hematologic changes induced by intravenous administration of diacetoxyscirpenol in pigs, dogs, and calves.

Diacetoxyscirpenol (DAS) was given IV to pigs (0, 0.5, and 1.0 mg/kg of body weight), cattle (0 and 0.5 mg/kg), and dogs (0 and 0.5 mg/kg). Blood was collected and hemograms were done at 0.5-hour intervals for 8 hours. The animals were euthanatized at 8 hours after treatment, and bone marrow samples were taken and examined by light microscopy. Moderate to severe necrosis of bone marrow hematopoietic elements was found in animals given DAS. The sequential increase in the type and number of abnormal cells in the blood suggested a successive destruction of the hematopoietic elements. A marked left shift in the neutrophil population was found in animals given DAS. Metarubricytes and large platelets were found in the blood of animals given DAS. Lymphocytes were replaced with immature cells. Pathologic changes were most severe in the pigs given a dosage of 1.0 mg of DAS/kg. The order of species sensitivity to DAS was pigs greater than dogs much greater than cattle.

Animals↗
PubMed1988

Experimental T-2 toxicosis in swine following inhalation exposure: clinical signs and effects on hematology, serum biochemistry, and immune response.

Nine- to ten-week-old, male castrated, specific pathogen-free derived pigs, weighing 34 to 42 kg, were exposed to a T-2 toxin aerosol (390 micrograms/liter, 1.5 microM mass median aerodynamic diameter) for a time period which allowed an amount equivalent to 8 mg/kg to be nebulized (six pigs). Control animals (five pigs) were exposed to an equivalent amount of the nebulized vehicle. Pigs were immunized subcutaneously with sheep red blood cells on Days 0 and 21. Whole blood and serum samples were taken periodically for clinical pathologic and immunologic studies. Pigs were closely observed, and daily rectal temperatures and weekly weights were measured. The T-2-treated pigs vomited and exhibited cyanosis, anorexia, lethargy, lateral recumbency, slightly elevated rectal temperature, and depressed body weight gain. The lymphocyte count decreased while the neutrophil count increased. The concentrations of total serum protein and hemoglobin declined. There was a marked increase in serum alkaline phosphatase activity on Day 1, followed by a marked and persistent decrease. Mitogen-induced (Con A, PHA, and PWM) blastogenic responses of peripheral blood mononuclear cells and hemagglutination titers to SRBC were also transiently decreased. Thus, inhalation exposure of pigs to a sublethal dose of T-2 toxin caused clinical signs of toxicity and adverse effects on clinical pathologic parameters and immune responses; however, most of these effects were short-lived. The changes described in our study resemble those reported in pigs given T-2 toxin by intravascular injection.

Administration, Inhalation↗
PubMed1988

The role of intestinal microflora in the metabolism of trichothecene mycotoxins.

The role of faecal and intestinal microflora on the metabolism of trichothecene mycotoxins was examined in this study. Suspensions of microflora obtained from the faeces of horses, cattle, dogs, rats, swine and chickens were incubated anaerobically with the trichothecene mycotoxin, diacetoxyscirpenol (DAS). Micro-organisms from rats, cattle and swine completely biotransformed DAS, primarily to the deacylated deepoxidation products, deepoxy monoacetoxyscirpenol (DE MAS) and deepoxy scirpentriol (DE SCP). By contrast, faecal microflora from chickens, horses and dogs failed to reduce the epoxide group in DAS and yielded only the deacylation products, monoacetoxyscirpenol (MAS) and scirpentriol (SCP), in addition to unmetabolized parent compound. Intestinal microflora obtained from rats completely biotransformed DAS to DE MAS, DE SCP and SCP; and T-2 toxin to the deepoxy products, deepoxy HT-2 (DE HT-2) and deepoxy T-2 triol (DE TRIOL). Rat intestinal microflora also biotransformed the polar trichothecenes, T-2 tetraol and scirpentriol, to their corresponding deepoxy analogues. Deepoxy T-2 toxin (DE T-2) was synthesized from T-2 toxin and demonstrated to be 400 times less toxic than T-2 toxin in the rat skin irritation bioassay and non-toxic to mice given 60 mg/kg ip, demonstrating that epoxide reduction is a significant single step detoxification reaction for trichothecene mycotoxins.

Animals↗
PubMed1988

Tissue residues of diacetoxyscirpenol in pigs and calves after intravenous dosing.

Pigs (n = 19) were given 0, 0.1, 0.5, or 1 mg of diacetoxyscirpenol (DAS)/kg of body weight, and heifers (n = 7) were given 0 or 0.5 mg of DAS/kg. Animals were anesthetized and exsanguinated 8 hours after administration of DAS, and liver, kidney, skeletal muscle, mesenteric lymph node, and spleen were analyzed for DAS. Diacetoxyscirpenol was not detected in tissues from animals not given DAS. All tissues from pigs and calves given DAS contained at least traces (less than or equal to 10 ng/g of tissue) of DAS.

Animals↗
PubMed1987

Metabolism of three trichothecene mycotoxins, T-2 toxin, diacetoxyscirpenol and deoxynivalenol, by bovine rumen microorganisms.

The three trichothecene mycotoxins T-2 toxin, diacetoxyscirpenol (DAS) and deoxynivalenol (DON) were incubated in vitro for 12, 24 and 48 h with rumen microorganisms obtained from a fistulated dairy cow. Gas chromatographic and gas chromatographic-mass spectrometric analyses of extracts indicated all three toxins were biotransformed to a variety of deepoxy and deacylated products. DON was partially converted to a product identified as deepoxy DON. DAS was rapidly converted to four products including 15-monoacetoxyscirpenol (MAS), scirpentriol and two new compounds identified as 15-acetoxy-3 alpha,4 beta-dihydroxytrichothec-9,12-diene (deepoxy MAS) and 3 alpha,4 beta,15-trihydroxytrichothec-9,12-diene (deepoxy scirpentriol). T-2 toxin was also completely biotransformed to the products HT-2, T-2 triol and two new metabolites identified as 15-acetoxy-3 alpha,4 beta-dihydroxy-8 alpha-(3-methylbutyryloxy) trichothec-9,12-diene (deepoxy HT-2) and 3 alpha,4 beta,15-trihydroxy-8 alpha-(3-methylbutyryloxy)trichothec-9,12-diene (deepoxy T-2 triol).

Animals↗
PubMed1987

Therapeutic efficacy of superactive charcoal in rats exposed to oral lethal doses of T-2 toxin.

Superactive charcoal, a compound known to complex with many toxins, was evaluated in this study for its effectiveness in preventing death in rats given an oral lethal dose of 8 mg/kg body weight of T-2 toxin. The median effective dose of oral superactive charcoal in preventing deaths in rats was 0.175 g/kg body weight. Concurrent use of cathartics, such as sorbitol, magnesium sulfate and sodium sulfate, to facilitate removal of the superactive charcoal:T-2 toxin complex formed in vivo did not enhance the survival rates of rats. One gram per kilogram body weight oral superactive charcoal enhanced survival times and survival rates in rats given 8 mg/kg of T-2 toxin as late as 3 hr after the T-2 toxin was administered. Some benefit in survival rate may be derived from giving the superactive charcoal as late as 5 hr after the T-2 toxin.

Administration, Oral↗