Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eight mares were infected with equid herpesvirus-1 subtype 1 isolated from a case of equine paresis. In two mares killed at 4 d.p.i. immunofluorescence showed endothelial cell infection together with thrombosis in the rete arteriosus of the nasal mucosa and also in the spinal cord of one of these mares. Circulating platelet counts in the other six mares fell as early as 2 d.p.i. and remained depressed for seven days. Circulating immune complexes started to appear at 2 d.p.i., reached maximum levels at 10 d.p.i., but were undetectable at 28 d.p.i. Three of the six remaining mares developed varying degrees of inco-ordination at 8 and 9 d.p.i. In the two inco-ordinate mares that were killed at 9 and 10 d.p.i. the haemorrhages in the spinal cord and brain were associated with extensive endothelial cell fluorescence and thrombus formation. Clinical paresis coincided with an increase in circulating complement fixing and neutralising antibodies which in all six mares were higher against the subtype 2 isolate than subtype 1. In five yearlings infected with a subtype 2 isolate of EHV-1 platelet counts remained normal and neither immune complexes nor viraemia, nor inco-ordination were detected.
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PMID:Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: equine stroke. 301 74

Eleven isolates of equine herpesvirus-1 (subtype 1) all infected the brain following intracerebral inoculation of 2 d.o. mice. Most isolates were from cases of paresis, abortion or respiratory disease in the U.K., but established strains were also included. They divided into two subgroups. The 5 less pathogenic isolates were characterized by being restricted predominantly to the olfactory lobes. The 6 pathogenic isolates included the three known to cause equine paresis and were detected in neurones throughout the brain as well as giving rise to viraemia and infecting bronchial and renal epithelium and lymphoid cells in the spleen. Five respiratory isolates of subtype-2 were not recovered from inoculated mice.
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PMID:The pathogenicity in mice of respiratory, abortion and paresis isolates of equine herpesvirus-1. 631 Aug 51

Two young female rabbits (Oryctolagus cuniculus var. edulis) were inoculated subcutaneously with Bhanja virus (BHA) in a dose of 85 intracerebral LD50 for suckling mice (SMicLD50) and 8500 SMicLD50 (rabbit A and B, resp.). In rabbit A no clinical symptoms, nor viremia were observed, only seroconversion was revealed on day 7 p.i. On the other hand, in the rabbit B hypothermy on days 7--11 p.i., a mild adynamia on day 11 p.i. and a slight paresis on one hind leg on days 23--30 p.i. were observed; traces of BHA virus in the blood were detected on day 9 p.i. and seroconversion on day 7 p.i. The virus was not isolated from the interior organs (brain, liver, spleen, kidneys, lungs and heart) of the two rabbits dissected 38 days p.i.
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PMID:Experimental infection of rabbit with Bhanja virus. 722 74

Assessment of neurovirulence is a standard test for vaccines derived from virulent neurotropic viruses. This study evaluated the potential neurovirulence of V3526, a live attenuated vaccine derived from a full-length infectious clone of Venezuelan equine encephalitis virus (VEEV) Trinidad donkey strain (TrD), a comparator VEEV vaccine (TC-83), TrD, and process control material (PCM) in juvenile rhesus macaques. Following intrathalamic/intraspinal (i.t./i.s. ) or subcutaneous (s.c.) inoculations, animals were observed for periods of 18, 91 or 181 days for paresis, paralysis, neurological disorders and other signs of clinical illness. Blood was collected for measurement of viremia, VEEV neutralizing antibodies, hematologic parameters, and liver enzymes. Gross necropsies and histopathological examinations were conducted with emphasis on detecting lesions in the brain and spinal cord. Elevated temperatures (1-2 degrees C) were noted in several of the TrD and vaccine inoculated animals on Day 6 following inoculation and mean temperatures for the V3526 i.t./i.s. and TC-83 groups were higher than PCM group throughout the study Day 18. No significant differences were seen for weight or clinical chemistry results between vaccine and PCM inoculated groups. Clinically significant signs (Grades 3 or 4) were noted in three of 21 V3526 i.t./i.s. and three of 12 TC-83 inoculated animals, however, these signs resolved within 3 weeks for all V3526 i.t./i.s. and for two of three TC-83 inoculated animals. At Day 18 extensive lesions indicative of a viral infection were seen in brain sections of all four TrD inoculated animals and one of seven V3526 i.t./i.s. inoculated animals. Only scattered lesions, characterized by foci of gliosis and vessels with perivascular inflammation, were found in the sections from four TC-83 and six V3526 i.t./i.s. inoculated animals. The minimal histological changes observed at Day 18 resolved to baseline levels by Day 181 comparable to the PCM group. V3526 was immunogenic and essentially nonneurovirulent when administered via the clinically relevant subcutaneous route.
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PMID:Neurovirulence evaluation of Venezuelan equine encephalitis (VEE) vaccine candidate V3526 in nonhuman primates. 1850 63

The arterivirus lactate dehydrogenase-elevating virus (LDV) causes life-long viremia in mice. Although LDV infection generally does not cause disease, infected mice that are homozygous for the Fv1(n) allele are prone to develop poliomyelitis when immunosuppressed, a condition known as age-dependent poliomyelitis. The development of age-dependent poliomyelitis requires coinfection with endogenous murine leukemia virus. Even though LDV is a common contaminant of transplantable tumors, clinical signs of poliomyelitis after inadvertent exposure to LDV have not been described in recent literature. In addition, LDV-induced poliomyelitis has not been reported in SCID or ICR mice. Here we describe the occurrence of poliomyelitis in ICR-SCID mice resulting from injection of LDV-contaminated basement membrane matrix. After exposure to LDV, a subset of mice presented with clinical signs including paresis, which was associated with atrophy of the hindlimb musculature, and tachypnea; in addition, some mice died suddenly with or without premonitory signs. Mice presenting within the first 6 mo after infection had regions of spongiosis, neuronal necrosis and astrocytosis of the ventral spinal cord, and less commonly, brainstem. Axonal degeneration of ventral roots prevailed in more chronically infected mice. LDV was identified by RT-PCR in 12 of 15 mice with typical neuropathology; positive antiLDV immunolabeling was identified in all PCR-positive animals (n = 7) tested. Three of 8 mice with neuropathology but no clinical signs were LDV negative by RT-PCR. RT-PCR yielded murine leukemia virus in spinal cords of all mice tested, regardless of clinical presentation or neuropathology.
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PMID:Poliomyelitis in MuLV-infected ICR-SCID mice after injection of basement membrane matrix contaminated with lactate dehydrogenase-elevating virus. 2233 Mar 47