PubMed Health⌕ Search

Biomedical subjects

W C Edwards

Publications and source records attributed to W C Edwards.

At least 19 recordsLinked to original sources
PubMed1992

A case of monensin poisoning in ostriches.

A clinical case of monensin poisoning in ostriches is presented. Analytical results and histopathologic changes in intercostal muscles and liver supported the ionophore toxicity diagnosis.

Animals↗
PubMed1991

Aldicarb toxicosis in a dairy herd.

Aldicarb, an extremely toxic carbamate, caused sudden death of several lactating Holstein cows. Confirmation of this toxic agent as the cause of death was hindered by its rapid breakdown in biological tissue. Therefore, aldicarb was not detected in rumen contents of some of the dead cows, and brain acetylcholinesterase values were essentially normal. The analyses were conducted 2 to 4 days after death of the cows. Rapid testing of tissue samples is necessary if a carbamate insecticide is suspected.

Aldicarb↗
PubMed1991

Investigating oiled birds from oil field waste pits.

Procedures and results of investigations concerning the oiling of inland raptors, migratory water-fowl and other birds are presented. Freon washings from the oiled birds and oil from the pits were analyzed by gas chromatography. In most instances the source of the oil could be established by chromatographic procedures. The numbers of birds involved (including many on the endangered species list) suggested the need for netting or closing oil field waste pits and mud disposal pits. Maintaining a proper chain of custody was important.

Animals↗
PubMed1991

Livestock poisoning from oil field drilling fluids, muds and additives.

The use and potential toxicity of various components of oil well drilling fluids, muds and additives are presented. Many components are extremely caustic resulting in rumenitis. Solvent and petroleum hydrocarbon components may cause aspiration pneumonia and rumen dysfunction. Some additives cause methemoglobinemia. The most frequently encountered heavy metals are lead, chromium, arsenic, lithium and copper. Considerations for investigating livestock poisoning cases and several typical cases are reviewed.

Animals↗
PubMed1991

Sorption of sodium hydroxide by type I collagen and bovine corneas.

There are no quantitative studies on the uptake of alkali into corneal tissues. To study this phenomenon, both type I collagen and bovine corneas were incubated in sodium hydroxide (NaOH) under varying conditions for periods up to 27.5 h. The sorption (absorption or adsorption) of the alkali to protein and tissue was measured as the quantity of NaOH no longer available for titration to neutrality with hydrochloric acid. Sorption was found to be dependent on the concentration of NaOH (0.01-1 N) but independent of the incubation temperature (4-35 degrees C). In whole cornea, sorption of 1 N NaOH began immediately and increased with time up to 6 h. After 6 h, sorption decreased, together with the observed degradation and solubilization of the tissue. Stripping of the corneal endothelium alone or of the endothelium and epithelium increased sorption in a similar manner when compared to whole corneas for periods up to 4 h. These observations are compatible with ionic and nonionic bonding of hydroxide ions to collagen (including that of the cornea) and the subsequent release of hydroxide ions during hydrolysis of the protein itself. Indirect evidence also suggests the inclusion of quantities of unbound hydroxide ions in hydrated gels of glycosaminoglycans. It is proposed that in a chemical burn of the cornea, alkali is both stored in the tissue (by sorption) and reacted with it (by hydrolysis), without any net consumption of alkali taking place.

Absorption↗
PubMed1989

Selenium toxicosis in three California sea lions (Zalophus californianus).

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.

Animals↗
PubMed1989

Toxicology of oil field wastes. Hazards to livestock associated with the petroleum industry.

In oil-producing states, the proximity of livestock to drilling operations and production sites often results in poisoning of animals from ingestion of crude oil, condensate, salt water, heavy metals, and caustic chemicals. The heavy metals encountered most frequently are lead from pipe joint compound and arsenicals and chromates used as corrosion inhibitors. Numerous toxic and caustic chemicals are used in drilling muds and fluids. Crude oil and salt water spills are common occurrences around production sites. Pipeline breaks may result in exposure of livestock to crude oil or refined petroleum hydrocarbons. Ingestion of petroleum hydrocarbons may result in sudden death from peracute bloat. The most common cause of illness or death following exposure to petroleum hydrocarbons is aspiration pneumonia, which may cause a chronic progressive deterioration of health, with death after several days or weeks. Cases in which livestock are exposed to oil, salt water, or caustic chemicals, but do not die acutely or from aspiration pneumonia are more frustrating to diagnose. In these cases, parasitism, poor nutrition, and other debilitating diseases must be considered. Anorexia, weight loss, and decreased rumen motility may be caused by a disruption of normal rumen function. Petroleum hydrocarbons, salt water, and caustic chemicals have the potential of altering rumen flora and enzymatic processes as well as damaging the ruminal and gastrointestinal epithelium. The toxicity of petroleum hydrocarbons appears to be related more closely to the volatility and viscosity of the product than to other factors. The more volatile straight chain and aromatic petroleum hydrocarbons have a greater potential for aspiration pneumonia and may produce an anesthetic-like action if absorbed systemically. The more volatile petroleum hydrocarbons also are more irritating to skin and mucous membranes and appear to be more damaging to rumen flora. Treatment of petroleum hydrocarbon ingestion is aimed at preventing aspiration pneumonia and the animal's absorption of highly volatile components. Activated charcoal slurries and, in some instances, vegetable oil may be used to absorb the ingested petroleum or alter its viscosity to minimize absorption and aspiration. These procedures should be followed by the administration of rumenatories or saline cathartics to hasten the evacuation of the gastrointestinal tract. Chronic poor performance animals with anorexia and rumen dysfunction may respond to fresh rumen inoculant, intravenous glucose, and B-complex vitamins. Prognosis primarily hinges on whether or not aspiration pneumonia has occurred. Treatment of aspiration pneumonia rarely is effe

Animals↗
PubMed1988

Hypomagnesemic tetany of ruminants.

Hypomagnesemic tetany of ruminants is a noninfectious metabolic disorder that occurs in a wide range of nutritional and management conditions. This article considers its etiology and pathogenesis, clinical signs, clinical pathology and lesions, diagnosis, clinical management, prevention, and control.

Animals↗
PubMed1986

Hepatic enzyme changes in bovine hepatogenous photosensitivity caused by water-damaged alfalfa hay.

In the winter of 1983, practitioners reported extensive photosensitization in 7 herds of cattle. All herds had a history of having been fed water-damaged alfalfa hay. A cow from one herd was referred to the veterinary teaching hospital at Oklahoma State University. In this herd of approximately 40 adult Polled Herefords, all cattle had had some degree of clinical involvement over the past 4 to 6 weeks. Clinical signs included scaling and erythema of sparsely haired skin, muzzle, and teats, as well as icterus, anorexia, and weight loss. One cow died, and the remaining cattle recovered over an 8- to 10-week period after removal of the hay from the ration. In the referred cow, values for total and conjugated bilirubin, BUN, creatinine, sorbitol dehydrogenase, serum alkaline phosphatase, serum aspartate transaminase, and serum gamma-glutamyl transferase were higher than normal. In the herd of origin, extremely high serum gamma-glutamyl transferase values (180 to 1,400 IU/L) persisted (normal, 2 to 35 IU/L). Feeding the same alfalfa hay to 2 clinically normal cows reproduced the syndrome. The characteristic hepatic lesion was bile duct necrosis, with secondary bile duct hyperplasia.

Alkaline Phosphatase↗