Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A leucoencephalomyelitis in 6 goat kids 2 to 5 months old is described. The disease was characterised by fever, ataxia, posterior paresis, circling and hyperaesthesia progressing to prostration. The neural lesion was confined to the white matter of the cerebellum and posterior brain stem in 4 kids, but in 2 others the cervical spinal cord was the main site affected. The lesion was characterised microscopically by dense perivascular cuffing with mononuclear cells, infiltration of the parenchyma with macrophages and a proliferation of glial cells and by a marked primary demyelination. In more advanced lesions, areas of the neurophil were replaced by a loose glial scar. There were associated pulmonary lesions of interstitial pneumonitis and hyperplasia of the peribronchiolar lymphoid tissue. Attempts to isolate an aetiological agent and to transmit the disease to young goat kids and lambs were unsuccessful. The disease has not been reported before in Australia but has distinct similarities to an infectious leucoencephalomyelitis of young goats which has been described in North America.
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PMID:Leucoencephalomyelitis of goat kids. 74 45

We report a four-year-old boy with HIV encephalopathy after vertical HIV infection. On the first admission to our hospital he showed ataxia, loose of expressive language and interstitial pneumonia. After treatment of the pneumonia the patient was started on oral zidovudine with 6 x 6 mg/kg bw/day, because of persisting neurologic symptoms and deep white matter lesions in the MR tomogram of the brain. Two months later he showed an improvement of the gait and the reappearance of the expressive language. Seven months after the start with zidovudine the MR tomogram of the brain revealed the disappearance of white matter lesions with exception of little areas of demyelinisation. No side effects of treatment were observed. The only persisting pathological clinical signs were developmental delay of about a half year and moderately hyperactive tendon reflexes of the lower extremities. Our case suggests that even oral treatment with zidovudine can have a beneficial effect on the HIV encephalopathy in infants.
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PMID:[The effect of high-dose peroral zidovudine treatment in a 4-year-old child with HIV encephalopathy]. 156 Sep 90

The aim of the present investigation is the complex study of experimental infection in pregnant ewes by means of clinical, serological, biological, histological and Electron microscopy methods. Four ewes, pregnant from the 2nd to 5th month, were infected by intravenous (in one case by intraperitoneal) routes with a C. burnetii strain at 10(6) ID 50/ml. The clinical illness in all of the animals was characterized by fever and two-phase temperature reaction on the 5th and 12th days. The clinical symptoms were as follows: torpidity, reduced appetite, thirst, conjuctivitis, rhinitis, rapid breathing. As a result of the developed latent infection, after the acute stage, the animals gave birth to three unviable lambs who died within 24 h. Another lamb was still-born. The lambs showed cachexia, arthritis, ataxia, wrinkled skin. The highest CF-titers (1:256-1:512) were reached on the 40th day, but serum antibodies (1:8-1:32) first appeared on the 8th day. The titers began to decrease on the 60th day. The pathomorphological changes testify to a latent infection characterized by placentitis, lymphocellular proliferation of the lamb's parenchymal organs and lymph nodes, multiple thromboses, interstitial pneumonia and plural proliferative changes. The EM exam showed rickettsiae in placentas mainly in the form of inclusions in cytoplasm of leukocytes and epithelial cells.
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PMID:Experimental Q fever in sheep. 260 70

Intercurrent canine distemper and Tyzzer's disease were diagnosed in a mature raccoon (Procyon lotor) submitted for necropsy. Clinical, gross and microscopic findings characteristic of canine distemper virus (CDV), included ataxia, dyspnea, suppurative conjunctivitis, interstitial pneumonitis and generalized lymphocytolysis. Inclusion bodies typical of CDV infection were present in many epithelial tissues. Acute multifocal hepatic necrosis and acute segmental necrotizing enteritis were attributed to the presence of Bacillus piliformis organisms in these lesions, confirmed by special stains and electron microscopy. This is apparently the first reported case of Tyzzer's disease in a raccoon.
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PMID:Tyzzer's disease as a complication of canine distemper in a raccoon. 395 Oct 62

This report describes vaccine-induced canine distemper virus (CDV) infection in four European mink (Mustela lutreola) induced by the administration of a multivalent, avian-origin vaccine. Clinical signs consisting of seizures, ataxia, facial twitching, oculonasal discharge, hyperkeratosis of footpads, and anorexia developed 16-20 days postvaccination. Conjunctival smears from one animal were positive for CDV antigen by direct fluorescent antibody testing, confirming the clinical diagnosis. The four mink died 16-26 days postvaccination. Gross and microscopic lesions that were diagnostic for CDV infection included interstitial pneumonia, lymphoid depletion, nonsuppurative encephalitis, and dermatitis. Vaccine-strain virus was isolated from tissues of three animals. Cases of vaccine-induced distemper in mustelids using avian-origin vaccine have seldom been reported.
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PMID:Vaccine-induced canine distemper in European mink, Mustela lutreola. 936 45

Unusual clinical and pathological observations in the field in goats and sheep suffering from Strongyloides papillosus infection prompted experimental work on this parasite. Goats were infected percutaneously with either single or multiple, low or high levels of S. papillosus. Young goats up to 12 months of age were found to be the most susceptible. Some animals, however, showed substantial resistance to infective doses. Clinical signs included transient diarrhoea, misshapen, elongated faecal pellets terminally, dehydration, anorexia, cachexia, gnashing of teeth, foaming at the mouth, anaemia and nervous signs such as ataxia, a wide-based stance, stupor and nystagmus. A 'pushing syndrome' was seen in 22% of the animals. The pathological changes are described and included enteritis, status spongiosus in the brain, hepatosis leading to rupture of the liver, nephrosis, pulmonary oedema, interstitial pneumonia and pneumonia. About 6% of the goats died acutely from fatal hepatic rupture. The development of an acquired immunity was determined. The immunity elicited an allergic skin reaction at the application site of larvae or injection sites of larval metabolites. This immunity, however, could be breached by large doses of larvae. The most profound clinicopathological changes induced by the parasites were an anaemia (most pronounced in the young goats) and hypophosphataemia. Trace element analyses provided evidence of Cu, Mn and possibly Se deficiencies in some goats.
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PMID:Experimental studies with Stronglyloides papillosus in goats. 1063 9

A large Wisconsin mink (Mustela vison) farm experienced an outbreak of toxoplasmosis in the spring of 1999 following an outbreak of canine distemper during the previous fall. Major clinical signs for pregnant females included reduced feed consumption, abortions, and stillborn kits; kits < or =3 weeks old experienced ataxia and mortality. Of 7,800 females, 1,976 (26%) lost their entire litter either from abortion or neonatal mortality. Kit mortality from 7 days to 3 weeks of age was 3,300, and overall kit mortality attributed to the toxoplasmosis outbreak was 10,408. Six neonatal mink kits, 12 3-week-old kits, and 2 adult female mink were submitted to the University of Minnesota Veterinary Diagnostic Laboratory for diagnostic workup. Gross postmortem lesions were limited to empty stomachs (12 of 12 kits) and pale livers (4 of 12 kits) for the 3-week-old kits. Major microscopic lesions included interstitial pneumonia, encephalitis, encephalomalacia, and myocarditis. Toxoplasmosis was diagnosed by microscopic lesions, microscopic lesion distribution, and the detection of Toxoplasma gondii tachyzoites by immunohistochemistry. This is the first detailed report of an outbreak of toxoplasmosis in mink in the United States.
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PMID:An outbreak of toxoplasmosis in farmed mink (Mustela vison S.). 1148 3

Infection with Baylisascaris procyonis, the common roundworm of raccoons, was found to be the cause of an epizootic of fatal CNS disease in domestic rabbits (Oryctolagus cuniculus). Clinical signs included torticollis, ataxia, tremors, and falling. Gross lesions were limited to white, raised nodules (1 to 1.5 mm) on the epicardium, endocardium, and liver serosa, and they were found to be larval granulomas. Microscopic lesions included multifocal myocarditis, multifocal hemorrhagic tracks and associated necrosis and inflammation in the liver, multifocal eosinophilic myositis, focal nephritis, and mild interstitial pneumonia; larval granulomas were seen in the heart, liver, lung, and mandibular salivary gland. Lesions in the brain consisted of multifocal areas of necrosis and inflammation in the cerebrum, cerebellum, midbrain, and medulla, with accompanying perivascular leukocyte aggregates and neuronal and axonal degeneration. Large numbers of large ascarid larvae were seen in the brain. Epidemiologically, infection was linked to the use of contaminated straw from a barn used by raccoons. On the basis of this study as well as that of similar studies, it was concluded that barn use and contamination by raccoons may be an important source of infection of animals and possibly man with this parasite.
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PMID:Fatal cerebrospinal disease caused by Baylisascaris procyonis in domestic rabbits. 1200 87

Four pigs (group 1) were infected with an aerosol containing porcine reproductive and respiratory syndrome virus (PRRSV) followed 7 days later by pseudorabies virus (PRV). Three further pigs (group 2) received PRRSV alone, two (group 3) received PRV alone, and two (group 4) remained as uninfected controls. Despite the admittedly small numbers of animals, the experiment appeared to throw light on aspects of synergy. Thus, the group 1 pigs showed severe neurological signs characterized by ataxia and muscular tremors. Total cell numbers in the bronchoalveolar lavage fluid were increased in all PRRSV-infected pigs, and PRRSV antigen was detected in the alveolar macrophages. Total cell numbers in the cerebrospinal fluid of group 1 pigs were considerably greater than those demonstrated in group 3, but no PRV antigen was found. Pigs of groups 1 and 2 showed pulmonary lesions, characterized by interstitial pneumonia and PRRSV antigen immunolabelling. Non-suppurative encephalitis was found in five of the six pigs of groups 1 and 3. In particular, one group 1 animal had severe necrotizing encephalitis with intranuclear inclusion bodies and associated immunolabelling of PRV antigen. The other three group 1 pigs had prominent malacic lesions, with macrophages. These neuropathological findings strongly suggested that PRRSV infection in pigs enhances the severity of brain lesions caused PRV.
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PMID:Encephalomalacic lesions in pigs dually infected with porcine reproductive and respiratory syndrome virus and pseudorabies virus. 1551 36

We report a 60-year-old man with a 6-year history of tremor in his hands. He noted the onset of short of breath and gait disturbance in 1994; both of these symptoms were slowly progressive. Then recently he developed fever two months prior to the present admission. He was admitted to the rheumatology department of our hospital and neurological consultation was asked on December 13, 2000. On neurologic examination, he showed Gottron sign and fine crackle in both lungs. Pertinent neurological findings were bilateral dysmetria in finger-to-nose and heel-to-knee tests and a broad-based gait. In addition, he showed intention tremor in upper extremities more on the left. Romberg sign was positive. Deep tendon reflexes were decreased. Vibratory sensation was reduced at the wrists. The patient's hemoglobin was 11.1 g/dl, with a mean corpuscular volume of 92.0 fl. Vitamin B12 level was 190 (reference range, >230 pg/ml). Serum lactic acid, pyruvic acid and ceruloplasmin were slightly elevated. Chest X-ray showed interstitial pneumonia. Muscle biopsy showed grouping of small angular fiber. Brain MRI showed diffuse atrophy of the cerebral cortex and the cerebellum hemisphere. Thalamotomy did not improve his tremor. He was admitted again in November 2001. General worsening of his neurological findings was observed. IL2-receptor was markedly elevated. Serum anti-Hu, Yo and Ri antibodies were negative. An anaplastic carcinoma was found in his jejunum. He died from respiratory failure in February 2002. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had paraneoplastic syndrome. Other diagnosis entertained included MERRF, GSS, Ramsay Hunt syndrome, subacute combined degeneration, spinocerebellar degeneration. Majority of the participants thought that paraneoplastic syndrome was most likely. Post-mortem examination revealed poorly differentiated carcinoma in the small intestine. Myeline pallor was noted in the posterior and the lateral columns in the thoracic spine. Neuronal cell loss was observed in the Purkinje cell and granular cell layer in the cerebellum. Sural nerve demonstrated loss of myelinated fibers and grouping of small fibers. Neuropathological findings were consistent with Friedreich ataxia; nevertheless, no mutation was reported in frataxin in Japan. The neuropathologist concluded that neuropathological diagnosis was a spinocerebellar ataxia with neuropathological similarities to Friedreich ataxia.
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PMID:[A 60-year-old man with intention tremor as an initial symptom followed by cerebellar ataxia, peripheral neuropathy and dementia]. 1614 16


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