Neospora-associated bovine abortion in Northern Ireland.
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Abortion, Veterinary↗
Biomedical subjects
M Jeffrey
Publications and source records attributed to M Jeffrey.
Numbers of neurons in vacuolated and non-vacuolated neuroanatomical nuclei in bovine spongiform encephalopathy-affected brains.
Morphometric studies of the brains of seven Holstein-Friesian cows affected with bovine spongiform encephalopathy (BSE) and five control cows are reported. The numbers of neurons were counted in five selected neuroanatomical nuclei, namely the vestibular complex and red nucleus, both of which consistently show a high degree of neuronal perikaryonal vacuolation, the dorsal vagal nucleus, which shows inconsistent perikaryonal vacuolation, and the caudate and hypoglossal nuclei, which do not usually show vacuolation. The vestibular complex of BSE-affected cattle contained about half the number of neurons present in the controls. No statistically significant neuronal loss was demonstrated at other sites. These results confirm previous findings, showing that neuronal loss is a significant feature of BSE and may therefore contribute to the development of the clinical disease. No association was found between the duration of clinical signs and the number of remaining neurons or the extent of the vacuolation. However, the absence of such association should be viewed cautiously as there was substantial variation in neuronal populations between individuals.
Animals↗
Morphogenesis of amyloid plaques in 87V murine scrapie.
Amyloid plaques of scrapie-infected mouse brains are composed of fibrillar forms of a host coded, cell surface sialoglycoprotein called PrP (prion protein). Serial ultrastructural immunogold staining was performed on plaques identified by light microscopic immunocytochemistry of brains of VM mice infected with the 87V strain of scrapie. Classical plaques, of a kuru-type morphology, were composed of a central core of bundles of amyloid fibrils. Amyloid fibrils of classical plaques were immunoreactive for PrP. In addition, PrP was also found at the plaque periphery, in the absence of fibrils, at the plasmalemma of cell processes and in the associated extracellular spaces. Frequent microglial cells and occasional astrocytes contained PrP within lysosomes. Other plaques with few or no recognizable amyloid fibrils were frequent and were termed primitive plaques. PrP could be demonstrated in a non-fibrillar form at the plasmalemma and in the extracellular spaces between neurites of such plaques. Many primitive plaques showed little or no sub-cellular pathology associated with the PrP accumulation. PrP was closely associated with the plasmalemma of occasional dendrites passing towards the centre of primitive plaques. These results suggest that plaques are formed around one or more PrP releasing dendrites. PrP accumulates in the extracellular spaces adjacent to such processes prior to its spontaneous aggregation into fibrils. Lysosomal accumulation of PrP in microglia and astrocytes located at the periphery of plaques suggest that these cells are involved in the phagocytosis of excess or abnormal PrP.
Amyloid↗
Localization biopsy for impalpable breast lesions in a district general hospital.
127 patients undergoing localization biopsy for impalpable breast lesions were analysed retrospectively. Patients were included from both the UK Breast Screening Programme and from the symptomatic Breast Clinic. 49.6% of the biopsies were histologically benign, whereas 50.4% were malignant, including in-situ carcinoma. This is a significantly higher cancer rate than previous series. Localization biopsy has an important role in the diagnosis of mammographically suspicious lesions which are impalpable. 80% of the patients originated from the Breast Screening Programme which has important financial implications on surgical workload.
Adult↗
Bovine Neospora caninum abortion in the UK.
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Abortion, Veterinary↗
Conjunctival changes after subconjunctival lignocaine.
Subconjunctival injection of 2% lignocaine at the 12 o'clock position was used as the local anaesthetic in 19 eyes undergoing a primary trabeculectomy for open angle glaucoma. The appearance of the bleb and mean post-operative intraocular pressure (IOP) were compared with those in 29 eyes with the same diagnosis undergoing trabeculectomy under general anaesthesia by the same surgeons over the same time period. The two groups of eyes were similar with regard to treatment with beta blockers (p > 0.1), miotics (p > 0.25), sympathomimetics (p > 0.25), carbonic anhydrase inhibitors (p > 0.5), or no treatment (p > 0.25). Seventy-seven per cent of the local anaesthetic group and 25% of the general anaesthetic group developed avascular, thin-walled drainage blebs (p < 0.001). The mean post-operative IOP was significantly lower in the group receiving local anaesthetic (p < 0.001). The reasons for and significance of these observations are discussed, and the merits and disadvantages of thin-walled blebs are evaluated.
Adult↗
Ovine myeloencephalitis-leukomyelomalacia associated with a Sarcocystis-like protozoan.
Bilateral pelvic limb paresis developed in 7 of 15 10-month-old Blueface Leicester ram lambs on a mixed enterprise farm in the North of England. Clinical signs were principally mild to severe paresis of the pelvic limbs. Two mildly affected lambs recovered. Multifocal spinal cord white matter edema and necrosis, glial nodules, and mild to moderate nonsuppurative encephalomyelitis were the principal findings in 3 severely paretic lambs examined histologically. Protozoan bodies (12.7-23.0 microns) that stained immunocytochemically for Sarcocystis epitopes were in spinal cord glial cells of 2 of 3 lambs. Protozoa did not react immunocytochemically with anti-Toxoplasma gondii or Neospora canium antisera. Serology indicated there was recent exposure to Sarcocystis spp. in some surviving lambs. These cases resembled those in previous reports of paresis due to an unidentified Sarcocystis-like protozoan in sheep (ovine protozoan myeloencephalitis) in the British Isles, the USA, France, Australia, and New Zealand.
Animals↗
Pathology of renal dysplasia and bladder aplasia-hypoplasia in a flock of sheep.
Congenital renal disease was detected in a flock of sheep in the English Midlands over 2 successive years (1982 and 1983). A Suffolk ram was removed from the flock and test mated to unrelated Suffolk ewes in another flock; 14 of the resulting 43 lambs born in 1984 had an identical congenital renal disease. Kidneys were examined microscopically from 60 clinically affected neonatal lambs. Kidneys from 7 of the 60 clinically affected neonatal lambs (1, 1983; 6, 1984) were examined ultrastructurally and compared with kidneys from 3 healthy unrelated neonatal lambs. Most affected lambs examined (52/60) had bilaterally small kidneys (< or = 2 g) with fine intracortical cysts and distinct cortical and medullary zones. Kidneys were either grossly normal (3/60 lambs) or multicystic and of normal size to markedly enlarged (5/60 lambs). The bladder was absent or vestigial in most lambs. Microscopically, poorly differentiated ("primitive") tubules were present in renal cortex and medulla. Proximal convoluted tubules, where present, were formed by epithelial cells with distinctive round weakly autofluorescent intracytoplasmic inclusions with the ultrastructural appearance of atypical lysosomes. Loops of Henle, distal convoluted tubules, and juxtaglomerular-peripolar cell complexes were largely absent. Glomerular changes were minimal. Cystic dilatation of nephrons was restricted to proximal convoluted tubules lined by vacuolated epithelium. This distinctive congenital renal dysplasia of sheep was most likely inherited as a dominant trait with complete penetrance.
Animals↗
Immunodetection of a disease specific PrP fraction in scrapie-affected sheep and BSE-affected cattle.
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Amino Acid Sequence↗
Infection specific prion protein (PrP) accumulates on neuronal plasmalemma in scrapie infected mice.
Prion protein (PrP) is an abundant membrane-associated host protein which accumulates in abnormal, relatively protease-resistant forms in the brains of animals with scrapie and related diseases. Using correlative light and electron microscopy we determined the sites of subcellular localisation of PrP in mice infected with the 87V strain of scrapie. Disease specific accumulation of PrP was observed at light microscopy as amyloid plaques or as diffuse or granular staining within the neuropil, often clearly associated with individual neurons. Serial electron microscopical preparations were immunostained for PrP by the immunogold method. Gold particles were located on amyloid fibrils and on the plasmalemma of neurites at the periphery of plaques and in the neuropil, irrespective of the morphological form of PrP accumulation when viewed by light microscopy. This suggests that amyloid fibrils are formed following the accumulation and aggregation of sub-unit proteins at the plasmalemma and, furthermore, that normal PrP may be converted to its pathological form at this site.
Amyloid↗
Idiopathic brainstem neuronal chromatolysis and hippocampal sclerosis: a novel encephalopathy in clinically suspect cases of bovine spongiform encephalopathy.
Some of the brains submitted for neurohistopathological examination under the Bovine Spongiform Encephalopathy (BSE) Orders did not show lesions of BSE. They showed neuronal chromatolysis and necrosis of the brainstem, perivascular cuffs and meningeal infiltrates of mononuclear cells and large irregularly shaped vacuoles in the neuropil. About half of them also showed loss of pyramidal neurons in the hippocampus, with astrocytic gliosis. The topography of the brainstem neuronal degeneration and vacuolation was the same in all the cattle, suggesting that neuronal necrosis and chromatolysis, vacuolation and hippocampal sclerosis are part of a spectrum of changes common to a single disease. The cows affected with such changes came from most parts of Scotland with the largest number from the north east. They were of various breeds, mostly suckler cows, and were aged from six to 16 years. Some cows had had no reported access to feed supplements. Clinically, the cows showed a range of neurological signs: tremor, ataxia, apprehension and weight loss were described in more than 80 per cent of the cases. The cause of the disorder was not determined.
Age Factors↗
A neuropathological survey of brains submitted under the Bovine Spongiform Encephalopathy Orders in Scotland.
Bovine spongiform encephalopathy was not confirmed histologically in 225 of 829 bovine brains submitted for diagnosis. Several previously described disorders of the central nervous system were observed in these brains as well as disorders not previously recognised in Britain, including bilateral vacuolation of the substantia nigra, hippocampal sclerosis with brainstem neuronal chromatolysis and necrosis, focal symmetrical encephalomalacia and meningio-angiomatosis. Severe cerebellar dysplasia consistent with pre-natal bovine viral diarrhoea--mucosal disease virus infection or mineralisation of the blood vessels of the basal ganglia were interpreted respectively as congenital changes or changes due to ageing and were considered to be of no clinical significance.
Animals↗
A morphometric and immunohistochemical study of the vestibular nuclear complex in bovine spongiform encephalopathy.
A morphometric and immunohistochemical study of the vestibular nuclear complex was performed on five bovine spongiform encephalopathy (BSE) and five control cow brains. Neurons of the lateral and superior vestibular nuclei were counted at 500-microns intervals in 10-microns-thick sections, using an image analysis system comprising a projection microscope and digitising pad linked to a computer. A bimodal distribution of neuron diameters was recognised in the brains of normal cattle. One population of neurons had a mean diameter of 30 microns and the other had a mean diameter of 60 microns. The vestibular nuclei from BSE cattle had an approximately 50% reduction in total numbers of neurons when compared with controls (P < 0.01). Cattle which were clinically diseased longer had the fewest number of neurons preserved. Diminished numbers of neurons were detected throughout the area studied and affected neurons of all diameters. Immunohistochemical staining for synaptophysin, a protein present in synapses throughout the CNS, showed no significant reduction in axon terminals synapsing with vestibular neurons, including vacuolated neurons of BSE brains, when controls and BSE brains were compared. This suggests that de-afferentation of neurons is not the cause of neuronal loss. Prion protein was detected in the neuropil of the vestibular nuclear complex of BSE brains but not control brains. These studies show that previously unsuspected neuronal loss is a significant feature of BSE.
Animals↗
Ultrastructural features of spongiform encephalopathy transmitted to mice from three species of bovidae.
The ultrastructural neuropathology of mice experimentally inoculated with brain tissue of nyala (Tragelaphus angasi; subfamily Bovinae), or kudu (Tragelaphus strepsiceros; subfamily Bovinae) affected with spongiform encephalopathy was compared with that of mice inoculated with brain tissue from cows (Bos taurus; subfamily Bovinae) with bovine spongiform encephalopathy (BSE). As fresh brain tissue was not available for nyala or kudu, formalin-fixed tissues were used for transmission from these species. The effect of formalin fixation was compared with that of fresh brain in mice inoculated with fixed and unfixed brain tissue from cows with BSE. The nature and distribution of the pathological changes were similar irrespective of the source of inoculum or whether the inoculum was from fresh or previously fixed tissue. Vacuolation caused by loss of organelles and swelling was present in dendrites and axon terminals. Vacuoles were also seen as double-membrane-bound and single-membrane-bound structures within myelinated fibres, axon terminals and dendrites. Vacuoles are considered to have more than one morphogenesis but the structure of vacuoles in this study was nevertheless similar to previous descriptions of spongiform change in naturally occurring and experimental scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and kuru. Other features of the ultrastructural pathology of the transmissible spongiform encephalopathies including dystrophic neurites and scrapie-associated particles or tubulovesicular bodies were also found in this study. Neuronal autophagy was a conspicuous finding. It is suggested that excess prion protein (PrP) accumulation, or accumulation of the scrapie-associated protease-resistant isoform of PrP, may lead to localised sequestration and phagocytosis of neuronal cytoplasm and ultimately to neuronal loss.
Animals↗
Brain lesions of naturally occurring pregnancy toxemia of sheep.
The neuropathology and biochemical features of 17 sheep with clinical signs and gross necropsy features of naturally occurring pregnancy toxemia were retrospectively evaluated. The sheep ranged in age from 3 to 6 years and were of seven different breeds and three breed crosses. Thirteen sheep (case Nos. 1-4, 6-9, 11-14, 16) showed astrocytic nuclear swelling, hypertrophy and proliferation, and cerebrocortical neuronal necrosis. Seven of these sheep had Purkinje cell necrosis (case Nos. 2, 3, 6, 11, 12, 14, 16), and seven had vacuolation of cerebral and cerebellar sub-cortical white matter (case Nos. 1-4, 9, 12, 13). The neuropathologic features were similar to those of naturally occurring hypoglycemia of human beings and experimentally induced hypoglycemia of primates and the rat. The lesions seen in the sheep studied may have been caused by cerebral hypoglycemia, but data for blood or cerebral glucose concentrations were not available.
Animals↗
Evidence that bacteria are not causative agents of stunting syndrome in poults.
Two experiments were conducted to determine the effect of removing bacteria, including long segmented filamentous organisms (LSFO), from inoculum known to induce stunting syndrome (SS) in poults. Experiment 1 consisted of two identically designed trials. In each trial, each of four treatments was assigned to an isolator. Three treatments consisted of dosing, by crop intubation, groups of 1-day-old poults with unfiltered SS inoculum or filtrate of inoculum passed through .45- or .20-micron microfilters. Uninoculated poults were dosed with inoculum carrier, saline. Experiment 2 was done in battery facilities. Three rooms were used and each room housed one of three treatment groups. Triplicate pens of 10 poults each within each room were dosed by crop intubation with saline (uninoculated), unfiltered inoculum, or filtrate from .20-micron filtration. As compared with uninoculated poults, weight gain through 7 days was reduced 20% (P less than .05) by unfiltered and filtered inocula in both experiments. Jejunal maltase activity also was decreased (P less than .01) by unfiltered and filtered inocula. Feed efficiency (FE) was not determined in Experiment 1, but in Experiment 2, FE from 1 to 14 days of age was impaired by inoculum, irrespective of filtration. This effect was not evident during the 14- to 20-day period. The observation that the adverse effects of giving filtered inoculum to poults were the same as those caused by unfiltered inoculum indicated that bacteria, including LSFO, were not primary causative agents of the SS experimentally induced in poults.
Administration, Oral↗
Advanced uncontrolled glaucoma. Nd:YAG cyclophotocoagulation or tube surgery.
Forty-five patients with advanced uncontrolled glaucoma who had had noncontact neodymium:YAG (Nd:YAG) cyclophotocoagulation were matched and compared with 45 patients who underwent tube implantation surgery. The matching was based on selected criteria, including diagnosis, number of previous operations on the index eye, number of previous glaucoma operations, aphakia, vitrectomy, and age. The drop in intraocular pressure (IOP) was statistically significant in each of the 2 groups at 1, 4, 6, and 12 months of follow-up (P less than 0.001). The tube patients needed fewer antiglaucoma medications at 1 year (P less than 0.025) and more surgical intervention for IOP control, although this was not statistically significant (P greater than 0.1). Laser treatment was repeated in 49% of cases, and age younger than 40 years was identified as a risk factor for poor response to this mode of therapy. The effect on visual acuity and the expected complications also are discussed.
Adult↗
Scrapie inoculation of mice: light and electron microscopy of the superior colliculi.
Ultrastructural examination of the superior colliculi of mice intraocularly inoculated with the ME7 strain of scrapie showed vacuolation early in the course of infection. Brains were examined between 85-260 days after monocular inoculation with scrapie. The mean incubation period for the development of clinical disease was 302 days. Vacuolation was seen initially in the contralateral superior colliculus and subsequently in the ipsilateral colliculus. In coded trials light microscopical vacuolation was seen from 218 days but ultrastructural examination showed that sparse vacuoles were inconsistently present in either or both of the ipsilateral and contralateral colliculi from 85 days; frequent vacuoles were seen from 190 days. Scrapie-induced vacuoles were differentiated from vacuoles present in control tissue by the presence of loculation or by a limiting double membrane which showed protrusion or proliferation of the innermost lamella. Vacuolation was seen in neuronal perikarya, myelinated fibres, dendrites and axonal presynaptic terminals. Vacuoles of myelinated fibres were observed within myelin and possibly also in the inner tongue of oligodendroglial cytoplasm. Whorled membrane configurations were also seen. Tubulovesicular particles, 40 nm in diameter, were recognised in two scrapie-infected mice. It is suggested that some scrapie vacuoles arise as a result of incorporation of abnormal membrane into organelles, possibly mitochondria, in neuronal perikarya and neurites and probably also within oligodendroglial cytoplasm and myelin.
Animals↗