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Biomedical subjects

G D Osweiler

Publications and source records attributed to G D Osweiler.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of zearalenone on various components of rabbit uterine tubal fluid.

A study was conducted to determine whether an orally administered mycotoxin, zearalenone (11.5 mg/kg of body weight/day), enters the uterine tubal fluid (UTF) of rabbits and to evaluate its influence on certain constituents of UTF. Using high-performance liquid chromatography, the concentration of zearalenone in UTF was maximal on day 1 of initial exposure to the compound, then decreased rapidly to half the peak concentration by day 5. The disappearance curve for zearalenone in UTF was linear throughout the treatment period (10 days) and was not detectable within 3 days after the last administration of zearalenone and the initiation of pregnancy (does were bred on day 10 of the zearalenone treatment). Zearalenone increased the volume of UTF (P less than 0.05) in estrous does, but decreased the pH (P less than 0.05) and the total free amino acid concentration (P less than 0.05) of UTF, compared with pretreatment values. The concentrations of several trace elements and amino acids known to be of critical importance in early embryonic development were altered by zearalenone treatment and/or pregnancy. Gross developmental anomalies were not evidenced when fetuses were examined on days 28 to 30 of gestation. It was concluded that zearalenone or associated metabolites affect factors that influence fertility during the early preimplantation period. Furthermore, the analysis of UTF appears to be an effective screening method for assessing certain potential reproductive toxicants.

Administration, Oral↗
PubMed1988

In vitro evaluation of isolated turkey cardiac muscle function.

Turkey papillary muscles can function in an isolated chamber containing oxygenated, pH-regulated, modified Krebs-Henseleit solutions. Experiments were conducted for up to 6 hr without dimunition of muscle function. Our data indicate that different calcium concentrations affect muscle contraction and relaxation velocities, load values, and latencies. This controlled in vitro biological assay system can be used in further studies to evaluate species specific cardiac toxins or drugs.

Animals↗
PubMed1987

The effects of zearalenone on reproduction in swine. I. The relationship between ingested zearalenone dose and anestrus in non-pregnant, sexually mature gilts.

Ninety-nine sexually mature, non-pregnant gilts were checked for estrus daily with a mature boar and then allocated at estrus (D O) to receive 2 kg/d of a diet containing 0, 1, 5 or 10 ppm purified zearalenone between D 5 and 20 of the estrous cycle during two seasons of the year (winter and summer). None of the gilts exhibited any visual signs of "hyperestrogenism" and there was no effect of season on interestrous interval (P>0.05). A significant effect of zearalenone dose on inter-estrous interval was detected (P<0.001). Gilts receiving 0 or 1 ppm had similar inter-estrous intervals (21.0+/-0.3 and 21.5+/-0.8 d, respectively) whereas gilts receiving 5 and 10 ppm had extended cycles (29.2+/-2.9 and 32.7+/-3.3 d, respectively). Plasma progesterone concentrations at D 19 to 21 were higher in gilts with extended cycles (P<0.001) and corpora lutea (CL) were present at laparotomy. Some 86% of these retained CL underwent spontaneous regression resulting in the onset of estrus within the next 30 d. Fecal zearalenone concentrations rose during ingestion of contaminated diets and declined to pretreatment values within 2 d (1 ppm) to 8 d (10 ppm) of the cessation of treatment. These data show that feeding zearalenone at concentrations of 5 to 10 ppm from D 5 to 20 of the estrous cycle causes luteal maintenance and extended inter-estrous intervals. Spontaneous regression of these CL usually occurs within 30 d after zearalenone is removed from the diet. Fecal zearalenone analysis does not appear to be an effective method for determining prior exposure to zearalenone when carried out more than a few days following the last ingestion of zearalenone.

Journal Article↗
PubMed1986

Ochratoxicosis in Iowa swine.

Ochratoxicosis was diagnosed in 2 Iowa swine herds. In both cases, clinical signs consisted of increased urination and water consumption. Pale tan kidneys were found in affected pigs at necropsy. Histologic examination of renal tissue from an affected pig revealed diffuse tubular nephrosis and interstitial fibrosis. In both cases, ochratoxin A was detected by thin-layer chromatography in extracts of whole corn and ground complete feed. Ochratoxicosis was reproduced in swine with feed obtained in one of the cases.

Animal Feed↗
PubMed1986

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.

Acute Disease↗
PubMed1985

Aflatoxicosis in feedlot cattle.

Aflatoxicosis was diagnosed in lightweight feedlot cattle fed aflatoxin-contaminated cottonseed or gin trash. Clinical signs of hepatic damage and death were recorded for more than 200 of the 14,000 animals in a feedlot. Aflatoxin concentration in feedlot products fed to these cattle ranged from 96 to 1,700 ng/g. Diagnosis was based on the correlation of characteristic microscopic liver lesions, high concentration of aflatoxin in cottonseed feed products, and isolation and detection of aflatoxin B1 and aflatoxin M1 in urine and liver from affected calves. This report describes a large-scale outbreak of aflatoxicosis and demonstrates the need for careful quality control of feed products susceptible to aflatoxin contamination.

Aflatoxins↗
PubMed1985

Selenium toxicosis in swine.

Selenium toxicosis was diagnosed as the cause of fatal paralytic disease in a group of feeder pigs. Lumbar poliomyelomalacia and coronary band necrosis were the principal lesions. High selenium concentrations were detected in liver and kidney. Excessive selenium was traced to the premix added to the complete ration.

Animal Feed↗
PubMed1985

Levamisole toxicosis in swine.

Levamisole toxicosis occurred in swine in a commercial swine operation after the animals were mistakenly injected intramuscularly with levamisole. Clinical signs consisted of vomition, salivation, ataxia, recumbency and death. Surviving animals recovered completely within 24 to 48 hr.

Animals↗
PubMed1984

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.

Animals↗
PubMed1984

Plasma pentachlorophenol concentrations in calves exposed to treated wood in the environment.

Six calves were fed grain and hay from a pentachlorophenol (PCP)-treated feeder twice daily. Samples of blood were collected twice a week. Plasma PCP concentrations increased rapidly to a maximum of 1,086 microgram/L within 10 days. After the 3rd week, calves were denied access to the treated feeder; PCP values returned rapidly to near base line (before calves were fed from the treated feeder). After base-line plasma PCP values were reached, 4 of the 6 calves were housed in a total confinement building and exposed (by inhalation) to lumber that was commercially treated with PCP. The building itself was free of structural PCP-treated lumber. The ratio of building volume to treated wood surface was approximately 49 to 1. During the 3 weeks the calves were confined, PCP values did not increase and were markedly lower than those associated with oral exposure to treated wood. Oral dosing of calves with PCP in capsules--0.05 and 0.5 mg/kg--resulted in maximal plasma PCP values of 1,449 and 9,555 micrograms/L, respectively. Oral exposures (feeding from contaminated feeder; capsule) appeared to be more important than inhalation in causing increased plasma PCP concentrations in cattle. Exposure from these sources may be estimated by comparison with experimental values from dose-response studies. Feeding from treated feeders resulted in lower plasma PCP values than did dosing with 0.05 mg/kg daily.

Administration, Oral↗
PubMed1984

Acute monensin toxicosis in sheep: light and electron microscopic changes.

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.

Acute Disease↗
PubMed1983

Effects of T-2 mycotoxin on bovine serum proteins.

Mycotoxin T-2 (0.5 mg/kg of body weight) was administered orally to mixed-breed beef calves. Serum protein fractions, immunoglobulin (Ig) G, IgM, and several complement protein concentrations were studied in control and toxin-treated calves. Total protein, albumin, and globulin concentrations all decreased in toxin-treated calves as compared with that in controls. Similarly, the concentrations of alpha-, beta 1-, and beta 2-globulin fractions were reduced in the toxin-treated calves more than those in controls. The IgG and IgM values were lower in toxin-treated calves than those in the controls. Complement proteins Bbov (of the alternate pathway) and the 3rd component of complement were lower in the toxin-treated calves. The fragment of Bbov activation, B gamma 2, was increased after toxin treatment, indicating that activation of the alternate complement pathway was responsible for at least some of the reduction of the 3rd component of complement.

Animals↗
PubMed1982

The effect of T-2 toxin on the bovine immune system: cellular factors.

The effect of T-2 toxin, a Fusarium metabolite, on the bovine cellular defense (immune) system was evaluated during high levels, chronic administration. The administration of T-2 toxin to calves at the rate of 0.6 mg/kg/day was associated with significant depression of lymphocyte responses to mitogens and significant decreases in chemotaxic migration of neutrophils.

Animals↗
PubMed1982

Effect of T-2 toxin on the bovine immune system: humoral factors.

The effect of a Fusarium metabolite, T-2 toxin, on the bovine humoral immune system was explored during high-level, chronic administration. T-2 toxin administered to calves for 43 days at the rate of 0.6 mg/kg per day was associated with alterations of serum protein fractions, immunoglobulin levels, and C3 levels. Significant reductions in the levels of alpha, beta 1, beta 2, and gamma globulins, but not albumin, occurred after T-2 toxin administration. Likewise, a decline in C3 and serum immunoglobulin levels were evident. The levels of immunoglobulin M and immunoglobulin A, but not immunoglobulin G, in toxin-treated calves were significantly lower than control levels.

Animals↗
PubMed1978

Lead poisoning in feeder calves.

A group of 90 feeder calves was accidentally exposed to lead for approximately 30 days. The source of the intoxication was determined to be contamination of feed ingredients from a railroad car. Fourteen calves died and 8 more were clinically affected. Blood samples were obtained from 24 exposed calves (16 clinically normal and 8 intoxicated), and the samples were analyzed for lead, delta-amino levulinic acid dehydrase activity, and free erythrocyte porphyrin. Blood lead values ranged from 0.44 to 1.16 parts per million. Amino levulinic acid dehydrase activity was not affected enough to be of diagnostic value, whereas free erythrocyte porphyrin was increased dramatically and consistently in lead-exposed cattle.

Animal Feed↗
PubMed1978

Hemostatic function in swine as influenced by warfarin and an oral antibacterial combination.

Pertinent literature on naturally occurring hemorrhagic diseases in poultry and livestock were reviewed and compared with reports on recent outbreaks of a hemorrhagic syndrome in swine. Epizootiologic, clinical, and hematologic data from porcine hemorrhagic disease suggest vitamin K-responsive hypoprothrombinemia. In weanling pigs, the toxicity of warfarin was compared with that in swine given tylosin and sulfamethazine antibacterial combination versus those given warfarin only. Toxicosis was induced in weanling swine fed warfarin daily at dose level of 0.055 mg/kg of body weight. Approximately 5 days after feeding was started, signs of poisoning appeared: lameness, anorexia, subcutaneous hematomata, melena, and periarticular enlargement. Administration of warfarin at dose level of 0.017 mg/kg did not cause clinical toxicosis, and 0.028 mg/kg produced significant increases in one-stage prothrombin time (OSPT) and activated partial thromboplastin time (APTT), but no evidence of clinical bleeding. When tylosin-sulfamethazine antibacterial combination was fed at normal and high dose levels concurrently with warfarin at dose level of 0.017 mg/kg of body weight, increase of clotting time, OPST, or APTT did not occur due to antibacterial influence. The antibacterial combination fed alone did not produce changes in clotting time, OSPT, APTT, fibrinogen, total protein, differential leukocyte count, or packed cell volume.

Animals↗