Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previously unrecorded nervous disease in pigeons was investigated. The disease, characterized by paresis, paralysis of the extremities, head-shaking, and torticollis, is contagious and spreads slowly. The mortality rate of affected pigeons was very high. The disease appeared to spread among pigeon flocks in spring and summer. The predominant gross change in most cases examined was congestion of the visceral organs. Some cases had grayish spots on the pancreas and kidneys. The histologic changes are characterized by neuronal and myelin degeneration with mononuclear cell infiltration and perivascular cuffing. Degeneration of the parenchyma and marked congestion are prominent in the visceral organs. The causal agent, found to be a virus, produced pock lesions on chorioallantoic membranes of developing chick embryos and failed to aagglutinate chicken RBCs. Antisera against Newcastle disease virus and avian encephalomyelitis virus did not neutralize the isolated virus. The virus produced typical signs in experimentally inoculated pigeons.
 ...
PMID:Viral encephalomyelitis of pigeons: pathology and virus isolation. 54 2

Eastern equine encephalomyelitis (EEE) was the cause of heavy mortality in coturnix quail (Coturnix coturnix) reared commercially in South Carolina. The birds showed depression, tremor, and partial paralysis that advanced into complete paralysis, torticollis, and death within a few hours. The only consistent lesion on necropsy was a catarrhal enteritis in the duodenal area. The disease spread rapidly to all pens throughout the two houses on the farm in all birds over 2 weeks old, and mortality ranged from 40 to 90% in the various pens within the house. Total mortality exceeded 90,000 birds. Age groups on the farm ranged from 1 day to 8 weeks, at which time the birds went for slaughter. It appears that the initial infection was spread by cannibalism. EEE was diagnosed by isolating the virus in fertile eggs and suckling mice, with subsequent identification by complement-fixation. This is the first documented case of EEE in coturnix quail.
 ...
PMID:Eastern equine encephalomyelitis outbreak in coturnix quail. 69 63

The pathological and immunohistochemical findings of avian encephalomyelitis (AE) were described in various tissues of naturally infected pigeons of a flock from a outbreak in Turkey. Clinically, paresis, paralysis, circling movement and torticollis of the head associated with nervous signs were marked symptoms among the diseased pigeons. At necropsy, small or large white-greyish foci were detected in the pancreas, and erosive-ulcerative foci along with petechial hemorrhages in ingluves. Histopathologically, lesions in central nervous system, particularly in the cerebellum molecular layer, consisted of non-suppurative encephalomyelitis. Lesions in the pancreas revealed non-suppurative pancreatitis along with acinar degeneration and necrosis and/or lymphoid aggregations. Immunohistochemical staining of formalin-fixed, paraffin-embedded tissues was performed using a direct-fluorescein antibody technique with chicken anti-AE virus serum fluorescein isothiocyanate conjugate. Viral antigen was strongly stained in cytoplasm of epithelial cells of the exocrine glands, and neurons of the cerebral hemispheres and midbrain. In addition, viral antigen was also marked in the kidneys and tissues of the digestive system. Consequently, this article is, to our knowledge, the first report of natural AE in pigeons.
 ...
PMID:Avian encephalomyelitis in naturally infected pigeons in Turkey. 1522 70

Torticollis can be either congenital or acquired. Acquired torticollis is often the manifestation of an underlying central nervous system disorder. Acute painless torticollis should always raise suspicion of a posterior fossa tumor. Acute disseminated encephalomyelitis is an inflammatory demyelinating disease of the central nervous system involving the subcortical white matter, and to a lesser extent, the gray matter. The illness typically has a monophasic course characterized by a variable combination of fever, headache, meningismus, seizures, spasticity, cranial nerve palsies, ataxia, and psychosis. The course, although often clinically severe, is generally benign with most children making a full recovery. A toddler presenting with subacute painless torticollis as the only manifestation of acute disseminated encephalomyelitis is described. The authors believe the neck twist in this child represented a form of dystonia because of basal ganglia involvement. Torticollis has not been reported as a presenting or only sign of disseminated encephalomyelitis.
 ...
PMID:Torticollis as the only manifestation of acute disseminated encephalomyelitis. 2060 59

Atypical models of experimental autoimmune encephalomyelitis (EAE) are advantageous in that the heterogeneity of clinical signs appears more reflective of those in multiple sclerosis (MS). Conversely, models of classical EAE feature stereotypic progression of an ascending flaccid paralysis that is not a characteristic of MS. The study of atypical EAE however has been limited due to the relative lack of suitable models that feature reliable disease incidence and severity, excepting mice deficient in gamma-interferon signaling pathways. In this study, atypical EAE was induced in Lewis rats, and a related approach was effective for induction of an unusual neurologic syndrome in a cynomolgus macaque. Lewis rats were immunized with the rat immunoglobulin variable (IgV)-related extracellular domain of myelin oligodendrocyte glycoprotein (IgV-MOG) in complete Freund's adjuvant (CFA) followed by one or more injections of rat IgV-MOG in incomplete Freund's adjuvant (IFA). The resulting disease was marked by torticollis, unilateral rigid paralysis, forelimb weakness, and high titers of anti-MOG antibody against conformational epitopes of MOG, as well as other signs of atypical EAE. A similar strategy elicited a distinct atypical form of EAE in a cynomolgus macaque. By day 36 in the monkey, titers of IgG against conformational epitopes of extracellular MOG were evident, and on day 201, the macaque had an abrupt onset of an unusual form of EAE that included a pronounced arousal-dependent, transient myotonia. The disease persisted for 6-7 weeks and was marked by a gradual, consistent improvement and an eventual full recovery without recurrence. These data indicate that one or more boosters of IgV-MOG in IFA represent a key variable for induction of atypical or unusual forms of EAE in rat and Macaca species. These studies also reveal a close correlation between humoral immunity against conformational epitopes of MOG, extended confluent demyelinating plaques in spinal cord and brainstem, and atypical disease induction.
...
PMID:The extracellular domain of myelin oligodendrocyte glycoprotein elicits atypical experimental autoimmune encephalomyelitis in rat and Macaque species. 2565 38