Search PubMed⌕ Search

Biomedical subjects

A A Bickford

Publications and source records attributed to A A Bickford.

At least 19 recordsLinked to original sources
PubMed1995

Apoptosis as a cause of death in chicken embryos inoculated with Newcastle disease virus.

Eleven-day-old chicken embryos were inoculated by the allantoic route with the GB strain of Newcastle disease virus (NDV). At 0, 24, 36 and 42 h post-inoculation (p.i.), the brain and heart tissues were harvested for DNA extraction, and the thymus and the brain were fixed and processed for light and electron microscopy. At 42 h p.i., most of the embryos had died; however, no histopathological changes could be seen in the embryos at any stage of infection. DNA extracted from the brain cells started showing fragmentation at 24 h p.i., and from the heart muscle cells at 36 h p.i. Electron microscopy of the brain and thymus showed condensation of the nuclear chromatin, apoptotic bodies, various forms of crescent formation and some evidence of necrosis. Fragmentation of cellular DNA, crescent formation and apoptotic bodies are the typical signs of cells undergoing apoptosis. We suggest that apoptosis of the heart and brain is probably a cause of death of chicken embryos in acute Newcastle disease infection.

Animals↗
PubMed1993

Preliminary characterization of a pleomorphic gram-negative rod associated with avian respiratory disease.

An unidentified, pleomorphic, gram-negative rod (PGNR) bacterium has been isolated from domestic fowl with respiratory disease. The PGNR was isolated in 5% of turkey accessions and 3% of chicken accessions, primarily from the respiratory tract. Preliminary characterization of this organism included reviewing accession records, conducting cultural and biochemical tests, and analyzing cellular fatty acids. The PGNR was also compared with other bacteria capable of inhabiting the avian respiratory system. Biochemical and cellular fatty acid analysis failed to identify the organism, however all 14 isolates were similar.

Animals↗
PubMed1989

Association of Reoviridae particles in an enteric syndrome of poults observed in turkey flocks during 1988.

An enteric syndrome of turkey poults, characterized by enteritis, crop mycosis, intestinal changes (pale, thin-walled ballooning with watery contents), and rickets, occurred during 1988 in 74 turkey flocks from different farms belonging to 9 California turkey growers. The flocks ranged in size from 9,000 to 120,000 birds. Pools of intestine sections from 618 birds, representing 78 field cases, were examined. Histopathological examination of the intestines showed a mild to severe atrophy with a reduced depth of crypts, which was more prominent in the distal part of the small intestine. Viral isolation attempts with primary cell cultures of chicken embryo kidney cells were negative. Examination by electron microscopy of negatively stained intestinal specimens revealed the presence of Reoviridae particles of 58.8 to 80 nm in diameter. Enzyme-linked immunosorbent assay results on the intestinal pools for mammalian and group A avian rotaviruses were negative. A statistically significant relationship was found for the presence of Reoviridae particles in the intestines of 10-21-day-old birds. Of the 7 most common pathological conditions analyzed, 2, rickets and intestinal changes (thin-walled ballooning intestine with watery contents), showed a statistically significant association with the presence of Reoviridae particles.

Age Factors↗
PubMed1989

Role of harderian glands in resistance against Mycoplasma gallisepticum challenge.

Harderian glands of one-day-old chickens were surgically removed. At one week old, these chickens and controls from which these tissues were not removed, were vaccinated intranasally with a temperature-sensitive mutant of Mycoplasma gallisepticum. Humoral and local immunity were measured by means of antibody in sera and tracheal washings, respectively. Protection was measured by resistance to intra-air-sac challenge with the S6 strain of M gallisepticum. There was no discernible difference in either humoral or local antibody response between vaccinated chickens from which the glands had been removed and control birds. In addition, both groups were significantly protected against air-sac challenge compared with unvaccinated controls. These results indicate that removal of the Harderian glands neither affects the production of antibody to M gallisepticum, nor alters the effectiveness of temperature-sensitive M gallisepticum vaccination. The role that the Harderian glands play in resistance to M gallisepticum is therefore questioned.

Air Sacs↗
PubMed1986

Necropsy of chickens, turkeys, and other poultry.

Necropsy of dead or terminally ill birds is a key approach to disease diagnosis. It is important that one establish an orderly, consistent necropsy procedure and evaluate gross lesions as to their likely cause and significance. A very high percentage of farm flock poultry maladies can be diagnosed by gross lesions plus a few simple laboratory procedures, such as direct microscopy, Gram's stain, fecal flotation, and aerobic bacteriology.

Animals↗
PubMed1984

Assessment of the delayed neurotoxic potential of isopropyl triphenylphosphate using a nontraditional testing strategy.

The potential of isopropyl triphenyl phosphate (ITP) to produce delayed neurotoxicity in hens was examined using several techniques. ITP contained O,O,O-triphenyl phosphate (24%), O-o-isopropylphenyl O,O-diphenyl phosphate (25%), O,O-diisopropyl-phenyl O-phenyl phosphate (20%), O-o, p-diisopropylphenyl O,O-diphenyl phosphate (18%) and O-p-isopropylphenyl O,O-diphenyl phosphate (6%). Hens treated twice, 3 wk apart, with doses of ITP as high as 11.7 g/kg showed no clinical signs of delayed neurotoxicity and only mild signs of general toxicity. Furthermore, none showed even subtle neurohistologic changes suggestive of delayed neurotoxicity. ITP produced dose-dependent inhibition of hen plasma cholinesterase and brain neurotoxic esterase (NTE). The study was continued because NTE inhibition has been shown to be a reliable predictor of organophosphates that produce delayed neurotoxicity. ITP was administered prior to tri-o-tolyl phosphate (TOCP) challenge in order to determine if it altered development of TOCP delayed neurotoxicity. ITP neither enhanced nor reduced the onset or severity of neurotoxicity produced by TOCP. The time-course for brain and spinal cord NTE inhibition by ITP and TOCP were compared and found to be different. The maximum brain NTE inhibition produced by ITP (doses up to 11.7 g/kg) was never complete (always less than 90%), and spinal cord NTE inhibition was significantly less than that produced in the brain. In contrast, brain and spinal cord inhibition produced by 500 mg TOCP/kg were equal and greater than 90%. This testing regimen showed that ITP produced an effect on NTE at the biochemical level without producing clinical or neurohistologic abnormalities in treated hens. Furthermore, this biochemical effect was qualitatively different than that produced by the delayed neurotoxicant TOCP.

Animals↗
PubMed1981

Neurotoxicity of two organophosphorus ester flame retardants in hens.

Delayed neurotoxicity in hens was reported after the administration of several chlorinated alkyl phosphates. Neurotoxicity increased in a homologous series with the size and/or hydrophobic nature of substituents. In the present study the neurotoxicities of two commercial flame retardants, Fyrol PCF [tri(2-chloropropyl) phosphate] and Fyrol CEF [tri)beta-chloroethyl) phosphate], were compared in adult White Leghorn hens. When Fyrol PCF (10 ml/kg neat) was administered orally to four hens, no inhibition of plasma cholinesterase or brain neurotoxic esterase was evident 24 h later. Fyrol CEF (10 ml/kg neat) produced significantly greater inhibition of plasma cholinesterase (87.1%) and brain neurotoxic esterase (30.0%). Since neither compound produced greater than 75% neurotoxic esterase inhibition, they were not expected to produce delayed neurotoxicity in hens. This was verified in hens treated twice with Fyrol PCF (10 ml/kg neat) or Fyrol CEF (10 ml/kg neat) and observed for 6 wk. Neither group showed behavioral or histopathologic evidence of delayed neurotoxicity. Measurement of neurotoxic esterase correctly predicted the lack of potential of the two flame retardants to induce delayed neurotoxicity in hens.

Animals↗
PubMed1981

Time course for neurotoxic esterase inhibition in hens given multiple diisopropyl fluorophosphate injections.

Neurotoxic esterase has been useful for predicting delayed neurotoxicity after acute administration of organophosphorus esters. The present study determined how it could be used to predict neurotoxicity after 20 daily sc injections of 0.05 mg/kg diisopropyl fluorophosphate (DFP) in adult hens. Brain neurotoxic esterase activities were measured during the course of intoxication. No significant occurred after a single DFP injection but the level of inhibition gradually increased to a maximum of 54.3% after 20 injections. The time courses for inhibition of plasma cholinesterase, brain pseudocholinesterase and brain acetylcholinesterase were distinctly different from that for neurotoxic esterase and the former 3 enzymes reached a plateau of inhibition after 1 or 5 DFP injections. Walking behavior was regularly measured in treated hens and distinct motor impairment was first noted after 5 daily DFP injections. Brains, spinal cords and sciatic nerves were removed 24 hr after the last injection and examined microscopically. All hens exhibited central-peripheral distal axonopathy that was characteristic for organophosphate delayed neurotoxicity. Neurotoxicity developed in the absence of a high level of inhibition of neurotoxic esterase following multiple injections of DFP and the "critical" level neurotoxic esterase inhibition used to predict subchronic neurotoxicity may be lower than that used after single treatments.

Animals↗
PubMed1975

A report of fourteen spontaneous tumors of the guinea pig.

Fourteen guinea pig tumors were received by the Purdue University Animal Disease Diagnostic Laboratories over a period of 5 yr. Among them were 2 mammary gland adenocarcinomas, a mammary gland adenoma, a malignant mixed tumor of the mammary gland, a Schwannoma, 2 limpomas, an inflammatory polyp of the ear canal, a uterine fibroma, 3 trichoepitheliomas, an undifferentiated carcinoma, and a histiocytic lymphosarcoma. The pathologic features of these neoplasms were presented in this report.

Adenocarcinoma↗