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Biomedical subjects

F D Galey

Publications and source records attributed to F D Galey.

At least 37 records · Page 2Linked to original sources
PubMed1994

Type C botulism in turkeys: determination of the median toxic dose.

The median toxic dose (TD50) of type C botulinum in turkeys was determined using an up-and-down method for toxicologic testing. Birds were dosed intravenously with 10, 20, or 40 mouse lethal dose per kilogram body weight (MLD/kg) of type C botulism toxin and observed for 5 days. Administration of toxin resulted in acute death, posterior paresis, or no effect, depending upon the dose. The TD50 causing posterior paresis was calculated as 25.75 MLD/kg (confidence interval = 17.08-38.82 MLD/kg). Posterior paresis was identified as the principal sign associated with sublethal botulism toxicosis in turkeys. The resultant posterior paresis was similar to the clinical syndrome observed in an unsolved field investigation.

Aging↗
PubMed1994

Effect of time and storage temperature on cholinesterase activity in blood from normal and organophosphorus insecticide-treated horses.

Delays between time of sampling and time of testing are common; therefore, the length of time that blood can be stored at various temperatures was evaluated for effects on cholinesterase activity. Six horses were treated with 16 g of trichlorfon per os, 6 horses were treated with 15 g of dichlorvos per os, and 10 horses were untreated controls. The cholinesterase activity in whole blood from each horse was measured using an adaptation of the Ellman colorimetric method. The blood from each horse was then divided into 3 groups and stored at 5 C (refrigerated), 20 C (room temperature), or 38 C (incubated). Subsequent cholinesterase activities were measured daily and then at weekly intervals. The cholinesterase activities did not significantly increase or were measured daily and then at weekly intervals. The cholinesterase activities did not significantly increase or decrease (P > 0.05) in the blood from the untreated horses until after 1 week for any of the 3 temperature groups. The cholinesterase activities did not significantly increase or decrease (P > 0.05) in the stored blood from the trichlorfon-treated horses for 4 weeks in all 3 temperature groups. The cholinesterase activities significantly increased (P < 0.05) in the stored blood from the dichlorvos-treated horses after 1 week when the blood was refrigerated and by 24 hours when the blood was stored at room temperature or incubated. Therefore, blood from normal or organophosphate-treated horses can be used for cholinesterase evaluation for up to 1 week when stored at 5 C.

Animals↗
PubMed1993

Clinical and pathologic findings of blue-green algae (Microcystis aeruginosa) intoxication in a dog.

A healthy dog developed signs of lethargy and vomiting after ingesting water from a tide pool containing blue-green algae. Fulminant hepatic failure occurred, and the dog was euthanized 52 hours later. At necropsy, the liver was large, friable, and discolored a dark red. Histopathology showed hepatocyte dissociation, degeneration, and necrosis. The alga was identified as Microcystis aeruginosa, a known hepatotoxin. The intraperitoneal administration of lyophilized cell material from the bloom caused hepatic necrosis in mice.

Animals↗
PubMed1993

Chemical study of the hepatotoxins from Microcystis aeruginosa collected in California.

Four cyclic peptide toxins were purified and quantified from the aqueous extract of algal cell material utilizing high performance liquid chromatography, thin layer chromatography, and fast atom bombardment mass spectrometry. The cyclic peptide toxins appear to be similar structurally to hepatotoxins from previously identified blooms of the blue-green alga Microcystis aeruginosa.

Amino Acid Sequence↗
PubMed1993

Estrogenic activity in forages: diagnostic use of the classical mouse uterine bioassay.

The classical mouse uterine bioassay was evaluated and adapted for routine diagnostic use in response to requests for evaluation of forages suspected of being estrogenic. Forages were extracted in acetone or 10% ethanol in acetone (v/v). Extracts were mixed with ground corn-based mouse feed. Immature female mice (n = 3/group) were fed a total of 100 g of the ground feed for 5 days. Body weights were monitored before and after the trial. After 6 days, the mice were euthanized and uterine weights were determined. Mean uterine weights were compared using 1-way analysis of variance with preselected contrasts for individual means. Selected uteruses were fixed in 10% neutral buffered formalin for histologic examination. Control feeds, diethylstilbestrol (DES), estradiol, coumestrol, feeds with no reported estrogenic properties, and a feed that caused hyperestrogenism in cattle were tested. Moderate levels of estrogenic compounds resulted in dose-responsive uterine enlargements (10-270 ppm coumestrol over 5 days). Extremely high levels of estrogen frequently resulted in feed refusal and lack of uterine enlargement (10 ppm DES, 100 ppm estradiol). Diagnostically significant estrogenic activity was recovered from the feed known to have been estrogenic in cattle. The classical mouse uterine bioassay was relatively inexpensive, quick, repeatable, and capable of detecting clinically relevant coumestrol levels in hay.

Animal Feed↗
PubMed1992

The correlation between serum selenium and blood selenium in cattle.

The selenium (Se) concentration of paired blood and serum samples from cattle was determined by 2 methods: 1) atomic absorption spectroscopy using hydride generation (HG-AAS), and 2) inductively coupled argon plasma emission spectroscopy using hydride generation (ICP). Samples from 327 cattle were analyzed by HG-AAS, and samples from 344 cattle were analyzed by ICP. The data were examined by linear regression analysis, and the technique of inverse prediction was utilized to determine prediction intervals for estimating blood Se concentration from known serum Se concentration. The correlation coefficients, by simple linear regression of serum Se on blood Se, were 0.79 (r2 = 0.62) and 0.88 (r2 = 0.77) for the HG-AAS data and the ICP data, respectively. For the HG-AAS data, the inverse prediction formula for estimating blood Se when serum Se is known, at the 95% prediction interval, was [formula; see text]. For the ICP data, the inverse prediction formula for estimating blood Se when serum Se is known, at the 95% prediction interval, was [formula; see text]. The prediction intervals were quite wide, and the accuracy of estimating blood Se from a known serum Se was not useful for diagnostic purposes. The use of serum Se concentration to assess nutritional status of cattle with respect to Se does not appear to be appropriate.

Animals↗
PubMed1992

Toxicosis in dairy cattle exposed to poison hemlock (Conium maculatum) in hay: isolation of Conium alkaloids in plants, hay, and urine.

Cattle in two herds developed signs of bloating, increased salivation and lacrimation, depression, respiratory distress, ataxia, and death after ingestion of hay that contained large amounts of poison hemlock (Conium maculatum). Twenty of 30 Angus cows and calves were affected in the first herd (2 died). In the second herd, 5 of 30 Holstein heifers were affected (1 died). The Conium alkaloids, coniine and gamma-coniceine, were quantified in the hay, the plants from the responsible hayfield, and the urine of affected animals.

Alkaloids↗
PubMed1991

Clostridium botulinum type-C intoxication associated with consumption of processed alfalfa hay cubes in horses.

An episode of nervous system dysfunction was observed in horses on 17 premises in 4 counties of southern California. Thirty-eight horses were affected, and 31 of those died. The common clinical signs of disease in the affected horses were: increased appetite; anxious attitude; rythmic, intermittent muscle tremors in the area of the tricep muscles; decreased palpebral tone; mydriasis; small hard fecal balls; and tendency to become sternally recumbent with the neck extended. The temporal distribution of cases on all 17 premises suggested a relationship between exposure to a common batch of alfalfa hay cubes and manifestations of similar clinical signs of disease in affected horses. Fifteen horses were submitted for necropsy. Diagnosis of botulism was established on the basis of detection of type-C1 toxin in the feed, in intestinal contents of 1 horse, and in the liver of the aforementioned horse and another horse. Toxigenic strains of Clostridium botulinum type-C were isolated from intestinal contents of 5 affected horses, one of which also contained type-C1 and type-C2 toxins. Seven of 10 horses treated with type-C antitoxin and plasma obtained from horses hyperimmunized with C botulinum type-C toxoids survived.

Animal Feed↗
PubMed1991

Staggers induced by consumption of perennial ryegrass in cattle and sheep from northern California.

Staggers was diagnosed in sheep and cattle from the northern California coast. The diagnosis was made on the basis of history of ingestion of perennial ryegrass (Lolium perenne) stubble, clinical signs of transient ataxia, which was aggravated by stimulation, and nearly complete recovery after removal of ryegrass as the primary forage. Morbidity was high, but death did not occur in any affected animals. The toxic endophyte, Acremonium lolii, was in most lower leaf sheaths from the ryegrass. Injection of extracts of the ryegrass from affected farms into mice induced signs of toxicosis. Additionally, ryegrass from all 3 farms contained the tremorgenic mycotoxin, lolitrem-B.

Animal Feed↗
PubMed1991

Forage-related nitrate toxicoses possibly confounded by nonprotein nitrogen and monensin in the diet used at a commercial dairy heifer replacement operation.

Two clinically different episodes of nitrate toxicosis in heifers at the same dairy were evaluated to determine whether dietary supplements could have contributed to the confounding signs of illness. The first episode followed a 24-hour period of feeding mismanagement and resultant overconsumption of both a protein/nonprotein nitrogen supplement and a monensin supplement. This episode was characterized by ataxia, bloating, and death, without the classic clinical signs of dyspnea, salivation, cyanosis, and dark-colored blood, or the cardinal histologic changes of cyanosis, tissue staining, petechiations, or congestion. Approximately 5 weeks later, another episode developed, without the feeding mismanagement or the presence of supplements, and was characterized by classic signs of nitrate toxicosis along with response to methylene blue treatment. In both episodes, the feed source was the same, with high concentrations of nitrate. Heifers of both episodes had high ocular nitrate values, confirming the toxicoses. The difference was the availability of supplements. Calculation of exposure makes it unlikely that either the nonprotein moiety or the monensin moiety could have reached toxic values. However, the cell-level effects of monensin may have caused the animals to not display classic signs of nitrate toxicosis, confusing the diagnosis and treatment. This report demonstrates how field toxicosis can differ from reports of toxicoses caused by single etiologic agents. Practitioners must be aware of the potential for interactions between (and confounding by) commercially used feed components.

Animal Feed↗
PubMed1991

Black walnut (Juglans nigra) toxicosis: a model for equine laminitis.

Twelve light horse geldings developed laminitis within 8 to 12 h of being dosed by nasogastric tube with an aqueous extract of black walnut (Juglans nigra). Four of the 12 horses developed the severe signs of grade 3 laminitis (lame at a walk, refused to lift feet). Laminitis was accompanied by mild depression and limb oedema. There was no evidence of shock or colic. The horses developed neutropenia by 4 h after dosing with the extract, which shifted to a relative neutrophilia by 8 to 12 h. Minimal increases in plasma epinephrine and cortisol concentrations were suggested in severely affected horses. Severe laminitis was characterized by necrosis of dermal tips of dorsal primary epidermal laminae. A proliferative epithelial response in these laminae was distinguished by numerous mitotic figures and clusters of epithelial cells. This evidence suggests that black walnut toxicosis is not only a consistent clinical model, but is also a reliable clinico-pathological and pathological model for study of the pathogenesis and treatment of laminitis.

Animals↗