Search PubMed⌕ Search

Biomedical subjects

J F Edwards

Publications and source records attributed to J F Edwards.

At least 73 records · Page 4Linked to original sources
PubMed1989

Ovine arthrogryposis and central nervous system malformations associated with in utero Cache Valley virus infection: spontaneous disease.

Gross appearance and histologic lesions seen in 15 newborn lambs in an outbreak of congenital arthrogryposis with hydrocephalus or hydranencephaly (CAH) in Texas are described. Severe arthrogryposis with skeletal muscle hypoplasia was seen in limbs of affected lambs. Spinal column deformities were also present. Multiple central nervous system (CNS) malformations were present in CAH lambs including micrencephaly, cerebellar hypoplasia, micromelia, hydrocephalus, hydranencephaly, and porencephaly. Histologic lesions consisted primarily of areas of necrosis and loss of the paraventricular neuropil and motor neurons in the CNS and a resolving myositis with poorly developed myotubular myocytes in skeletal muscle. Seroepidemiologic studies on the flock and serologic data from heart blood taken from the stillborn affected lambs indicated that the outbreak was due to in utero infection with Cache Valley Virus.

Animals↗
PubMed1988

Disseminated sarcocystosis in a cat with lymphosarcoma.

Cysts of the protozoan Sarcocystis sp were found in skeletal and cardiac musculature in a 1.5-year-old cat with lymphosarcoma. The cat was FeLV-positive and had grossly visible neoplastic involvement of the spinal cord, mediastinum, bone marrow, and kidneys. Ultrastructural examination of the parasitic cyst wall suggested that the species in this case was different from that described in the only other reported case. It was hypothesized that immunosuppression from FeLV infection permitted an aberrant life cycle with encystment of Sarcocystis sp in this cat.

Animals↗
PubMed1988

Progressive ataxia in a Charolais bull.

A 20-month-old Charolais bull was referred for evaluation of progressive hind limb ataxia. Clinical findings suggested a neuroanatomic lesion caudal to T2. Postmortem histologic examination revealed multifocal, acellular, pale, eosinophilic plaques throughout the cerebellum, which were diagnostic for the disease progressive ataxia of Charolais cattle. This disease is presumed to have a hereditary transmission and is not commonly recognized in the United States.

Animals↗
PubMed1987

Vesicular exanthema of swine virus: isolation and serotyping of field samples.

Virus isolation was attempted from 262 field samples of vesicular material collected during the outbreaks of vesicular exanthema of swine in the U.S.A. from 1952-54. Using primary swine kidney culture, viral cytopathogenic agents were isolated from 76.3% of the samples. However, an overall recovery rate of 82.1% was obtained after samples negative in tissue culture were inoculated intradermally in susceptible swine. All vesicular exanthema of swine virus isolates were identified as serotype B51 using complement fixation and serum neutralization tests. Two isolates did not react with antisera to known vesicular agents of swine and failed to produce vesicles or clinical signs of disease upon inoculation in swine. One vesicular exanthema of swine virus isolate from tissue of equine origin was pathogenic for swine but produced limited vesiculation at the site of intradermalingual inoculation in the tongue of a pony infected experimentally. Type B51 virus was reisolated from lesions produced in the pony and the pony became seropositive for virus type B51.

Animals↗
PubMed1985

Chronic eosinophilic pancreatitis and ulcerative colitis in a horse.

A generalized debilitating disease in a horse was believed to be related to hypersensitivity to migrating strongyle larvae. The clinical signs included weight loss, diarrhea, and ulcers on all 4 coronary bands. The mare's condition deteriorated rapidly, so the mare was euthanatized and necropsied. The major histopathologic findings were chronic multifocal eosinophilic pancreatitis, hepatic portal fibrosis, biliary hyperplasia, and chronic ulcerative eosinophilic colitis. This case was similar to previously reported cases of chronic eosinophilic gastroenteritis in horses. Although the etiologic agent was not evident, the distribution and character of the lesions were consistent with a hypersensitivity response to migrating parasitic larvae, most probably Strongylus equinus.

Animals↗
PubMed1985

Megakaryocytic infection and thrombocytopenia in African swine fever.

Pigs infected with an African swine fever field isolate of modified virulence became acutely thrombocytopenic four to five days after the onset of fever and viremia. By eight days after inoculation, all pigs were thrombocytopenic. Immunofluorescence microscopy demonstrated that 2 to 10% of the megakaryocytes were infected. By 13 days after inoculation, platelet counts returned to within normal limits, and there was megakaryocytic hyperplasia despite a continued viremia. Secondary complications delayed the return of normal circulating platelet levels in some pigs. The clinical findings of African swine fever are discussed in light of the gross and histologic lesions.

African Swine Fever↗
PubMed1985

Platelet and fibrinogen kinetics in healthy and African swine fever-affected swine: [75Se]selenomethionine-labeling study.

Platelet and fibrinogen survival times were determined in healthy pigs and in pigs infected with African swine fever (ASF) virus. Cohort labeling with [75Se]selenomethionine was performed. The platelet survival time in healthy pigs was 5.3 +/- 0.7 days, and the fibrinogen survival time was 6.7 +/- 0.8 days. Early deaths and profound thrombocytopenia prevented calculation of accurate platelet and fibrinogen survival times in ASF virus-infected animals. The ASF virus-infected pigs died of extensive hemorrhage and effusions while thrombocytopenic; however, there was normal thrombocytopoiesis during infection, as measured by incorporation of the radionuclide into platelets. There was a slight decrease in plasma fibrinogen concentration when the platelet count decreased. A dysfunctional fibrinogen was present late in the infection.

African Swine Fever↗
PubMed1985

Mechanism of thrombocytopenia in African swine fever.

Pigs were inoculated with an African swine fever (ASF) isolate of moderate virulence, and the changes in the number of circulating blood platelets during infection were correlated with the appearance of antiviral antibody and fluctuations in total plasma hemolytic complement concentrations. Thrombocytopenia was detected by postinoculation days (PID) 7 and 8, and antiviral antibody was detected by PID 7, using an indirect immunofluorescence technique. The total hemolytic complement concentration was moderately and transiently decreased from PID 5 to 9, but was consistently low from PID 18 to 26. Pigs inoculated with an ASF virus isolate of greater virulence had a decrease in platelet counts on PID 6 and 7, and the total plasma hemolytic complement levels decreased in all pigs by PID 6 to 7. Antibody to ASF virus was not detected in pigs inoculated with the more virulent isolate. Pigs sensitized to ASF viral antigen with an inactivated-virus vaccine or by previous infection with ASF were challenge exposed. Sensitized pigs became clinically ill and thrombocytopenic by 24 to 72 hours earlier than did inoculated, nonsensitized pigs. Vaccinated pigs inoculated with homologous virus had lower blood virus concentrations than did nonvaccinated pigs. African swine fever virus-sensitized pigs inoculated with heterologous virus had a higher fatality rate than did nonsensitized pigs, and the pigs died peracutely, with only a few gross lesions in evidence. In vitro experiments demonstrated that ASF virus antigen induced platelet aggregation in platelet-rich plasma from recovered, nonviremic pigs. Viral antigen, antibody, or complement was not demonstrable on the surface of platelets from pigs inoculated with ASF virus isolate, by direct immunofluorescence testing.

African Swine Fever↗
PubMed1984

Coagulation changes in African swine fever virus infection.

Pigs were infected with highly virulent (Tengani '62), with moderately virulent (DR '79) African swine fever (ASF) virus, or with virulent hog cholera (HC) virus. Changes in platelet counts, selected coagulation assays and concentrations of factor VIII-related antigen (VIIIR:Ag) were monitored. Permeability of aortic endothelium was studied after the injection of Evan's blue dye on various days after infection with DR '79 ASF virus. Virulent ASF virus caused prolongation of the activated partial thromboplastin time (APTT), 1-stage prothrombin time, and thrombin clotting time as early as postinoculation day (PID) 4. These changes became progressively more severe until death. Both virulent HC and DR'79 viruses induced an increase APPT and thrombin clotting time at PID 3 to 4, only occasionally did the prothrombin time increased significantly (P less than 0.01). The APPT began to decrease on PID 7 and 8, but only DR'79-infected pigs lived long enough to regain a normal APTT. Infection by ASF viruses caused acute thrombocytopenia after PID 6 and platelet counts of HC virus-infected pigs decreased progressively from the onset of fever to levels of 1 to 2 X 10(5)/mm3 at PID 6 to 7. All ASF virus-infected pigs had an increase in VIIIR:Ag beginning at PID 3, with maximum increases at PID 6 to 7. Hog cholera virus infection did not cause consistent changes in levels of VIIIR:Ag. Pigs infected with DR'79 virus did not have increased vascular permeability to Evan's blue dye during infection; however, there was markedly decreased staining of the aorta after pigs became thrombocytopenic.

African Swine Fever↗
PubMed1983

Complete Freund's adjuvant-induced pneumonia in swine: a model of interstitial lung disease.

Intravenously administered complete Freund's adjuvant, emulsified in saline, induced a lesion in the porcine lung characterized by a disseminated histiocytic interstitial pneumonia, type II pneumocyte proliferation and granulomatous arteriolitis. In addition, there was a persistent increase in numbers of alveolar macrophages. The lesion was well developed in 7 days. The sequential development and early resolution of the light microscopic lesions was studied for a period of 21 days after inoculation. The administration of Freund's adjuvant induced a spectrum of lesions typical of many forms of interstitial lung diseases of man and domestic animals. The pig is a suitable host for the investigation of the pulmonary inflammatory response and the repair mechanisms involved in chronic lung disease produced by infectious agents or environmental antigens.

Animals↗
PubMed1973

Utilization of iron gallate and other organic iron complexes by bacteria from water supplies.

The degradation of four soluble organic iron compounds by bacteria isolated from surface waters and the precipitation of iron from these complexes by the isolates was studied. All eight isolates brought about the precipitation of iron when grown on ferric ammonium citrate agar. Three isolates were able to degrade ferric malonate, and three others degraded ferric malate with iron precipitation. Only three isolates, two strains of Pseudomonas and one of Moraxella, were able to degrade gallic acid when this was supplied as the sole carbon source. One strain of Pseudomonas was found to be active in degrading ferric gallate. Electron microscopy of cells of this bacterium after growth in ferric gallate as the sole carbon source yielded results indicating uniform deposition of the iron on or in the bacterial cells. Seven of the isolates could degrade the iron gallate complex if supplied with additional carbon in the form of yeast extract.

Alcaligenes↗
PubMed1972

Adsorption of colloidal iron by bacteria.

The adsorption of iron from a positive-iron sol by species of seven bacterial genera was examined by electron microscopy. All species precipitated the iron from the sol, and the bacterial cells became encrusted with iron. This was related to iron deposition in surface water supplies.

Adsorption↗
PubMedDate not supplied

The effects of ochratoxin A on postimplantation rat embryos in culture.

The mycotoxin, ochratoxin A (OA), is a potent in vivo teratogen. Studies were performed to determine the in vitro effects of OA on postimplantation rat embryos. Embryos were explanted from pregnant Sprague-Dawley rats on day 10 of gestation and were cultured (within the yolk sac) for 45 hr in gassed rat serum containing OA at concentrations between 0 and 300 micrograms/mL. Gross morphology, histopathology and protein and DNA content of embryos were evaluated. An OA concentration-dependent reduction in yolk sac diameter, crown-rump length, somite number count, and protein and DNA content was observed. Ochratoxin A treatment also resulted in an increase in the incidence of defective embryos. Malformations included: growth retardation, hypoplasia of the telencephalon, poor flexion, stunted limb bud development, underdeveloped sensory primordia and decreased mandibular and maxillary size. Histological examination demonstrated extensive OA-induced necrosis of embryonal mesodermal structures and neuroectoderm. Thus, the rat embryo in culture is a sensitive indicator of OA toxicity and may be useful for predicting developmental hazards associated with this mycotoxin.

Animals↗
PubMedDate not supplied

Chronic idiopathic inflammatory bowel diseases of the horse.

A review of reported cases of inflammatory bowel diseases (IBDs) of horses for which no etiology was identified included cases of granulomatous enteritis (GE), multisystemic eosinophilic epitheliotropic disease (MEED), lymphocytic-plasmacytic enterocolitis (LPE), and idiopathic eosinophilic enterocolitis (EC). The terms EC and MEED were both used to describe a disease in horses characterized by infiltration of intestine and extraintestinal tissues with eosinophils. We use EC to describe IBD characterized by only intestinal infiltration by eosinophils. Horses with GE, MEED, or LPE are usually examined because of weight loss and depression, but horses with EC are usually examined because of signs of abdominal pain. Typically, horses with IBD have low concentrations of serumal proteins, especially albumin, and fail to adequately absorb glucose or xylose. Antemortem diagnosis of IBD can only be made by histologic examination of affected intestine. In some cases, antemortem diagnosis is made from histologic examination of rectal mucosa obtained by biopsy. Suspected causes of IBD in the horse include abnormal immune response to bacterial, viral, parasitic, or dietary antigens. Most horses with IBD do not survive, but horses with EC are more likely than those with LPE, MEED, or GE to respond to treatment. Successful treatments of horses with IBD include resection of grossly affected intestine and administration of corticosteroids.

Animals↗