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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A spontaneous model of Purkinje cell degeneration in rats is described. Breeding data indicate that the condition is hereditary and not sex linked. The breeding colony has remained free of common murine pathogens, including parvovirus. In older rats with pronounced ataxia, the major lesions consisted of greatly reduced numbers or complete absence of Purkinje cells (PCs), particularly in the anterior lobe of the cerebellum. There was a decreased thickness and increased cellular density of the molecular layer and degeneration of the inferior olivary nuclei. Morphometric analysis indicated that the anterior lobes of affected rats were 52% smaller than those of normal rats. In young rats, before severe signs of ataxia had developed, microscopic changes were minimal. The preliminary findings are discussed in relationship to human cerebellar ataxias and mouse models of Purkinje cell degeneration.
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PMID:Preliminary characterization of hereditary cerebellar ataxia in rats. 131 3

Newborn ferrets were inoculated with Mink Enteritis virus (parvovirus). They developed a cerebellar hypoplasia and presented severe ataxia. Electrophysiological study by intracellular recordings in the cerebellar cortex demonstrates that in these ferrets, like in other mammals, Purkinje cells deprived from granule cell input during development remain multiply innervated by climbing fibers in the adult.
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PMID:Evidence for a multiple innervation of cerebellar Purkinje cells by climbing fibers in adult ferrets infected at birth by a mink enteritis virus. 304 Jan 86

Aleutian disease was diagnosed as the cause of posterior ataxia and paresis in domestic ferrets. Six serologically positive animals (four clinically affected and two unaffected) were investigated in detail and seven other clinically affected ferrets were also identified. The diagnostic findings included hypergammaglobulinaemia, histological lesions in the central nervous system and parvovirus-like particles in mesenteric lymph nodes. A wider serological survey of 446 animals owned by members of a ferret club revealed an incidence of 8.5 per cent seropositive animals.
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PMID:Aleutian disease in domestic ferrets: diagnostic findings and survey results. 823 11

In October 1989, an epizootic duckling disease with high mortality occurred in Taiwan. The disease was characterized by droopiness, inappetence, ataxia, ruffled feathers, and watery diarrhea. Affected ducklings were lame, were unable to stand, showed opisthotonos, and often died 3 or 4 days after the onset of the disease. Tolerant maturing ducklings displayed atrophic upper bills with a protruding tongue and became stunted as they reached maturity. No diagnostic histopathologic lesions were found in these ducklings. Fourteen parvovirus isolates, 33 duck viral hepatitis virus (DVHV) isolates, two adenovirus isolates, and two reovirus isolates were obtained and identified from more than 500 sick ducklings in the epizootic. The epizootic was diagnosed as a co-outbreak of duck parvovirus infections and duck viral hepatitis. The high mortality in ducklings and the bill atrophy syndrome were reproduced in ducklings by inoculating the parvovirus isolates alone. The epizootic was controlled by an emergency immunization program of ducklings with sera collected from recovered ducks or a bivalent inactivated vaccine composed of local DVHV and parvovirus isolates.
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PMID:Infectious bill atrophy syndrome caused by parvovirus in a co-outbreak with duck viral hepatitis in ducklings in Taiwan. 839 11

Cerebellar degeneration (abiotrophy) (CD) is a spontaneous and accelerated degeneration of one or several mature cerebellar neuronal cell populations and has been described in many domestic animals, especially in dogs, with numerous breed-related cases. In cats, CD is mentioned as a rare sporadic entity. Late onset CDs are exceptionally uncommon and only two cases are reported in young adults, both aged 18 months. This report describes clinical and pathological findings of a late onset feline CD in a 9-year-old male Persian cat. The cat was presented with a history of progressive ataxia lasting 2 years. Neurological examination revealed severe neurological deficits such as generalised and severe ataxia, hypermetria in all four limbs, and bilateral absence of menace response. The lesion was diffusely localised in cerebellum. On gross pathology, the cerebellum appeared of normal size and shape and kidneys were characterised by mild hyperaemia. Histologically, lesions were limited to the cerebellum and kidneys. In the cerebellum, all cerebellar folia of both hemispheres and the vermis were affected. Changes were characterised by severe and diffuse loss of Purkinje cells, loss of cellularity in the granular layer, mild astrogliosis associated with moderate hypertrophy of Bergmann's glia. Immunohistochemistry for feline parvovirus antigen revealed a negative result. Renal lesions consisted of chronic fibrosis associated with chronic interstitial nephritis. CD is a rare disease and occurs commonly in puppies or young animals, who are clinically normal at birth and usually develop neurological signs within a few weeks or months after birth. This report represents the first case of CD in a middle-aged cat.
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PMID:Late onset cerebellar degeneration in a middle-aged cat. 1678 80

Numerous cases of acute-onset progressive ataxia, hindlimb paresis and paralysis of unknown aetiology occurred during 1993 to 2003 in cheetahs (Acinonyx jubatus) within the European Endangered Species Programme (eep). This study describes the immunohistochemical investigation of a possible viral aetiology of the "cheetah myelopathy". Antibodies to feline herpesvirus type 1, canine distemper virus, canine parvovirus and Borna disease virus were applied to formalin-fixed and paraffin-embedded brain and spinal cord sections from 25 affected cheetahs aged between three-and-a-half months and 13 years. Using the avidin-biotin complex technique, none of the antibodies gave positive immunosignals in either the brain or the spinal cord tissue.
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PMID:Immunohistochemical screening for viral agents in cheetahs (Acinonyx jubatus) with myelopathy. 1705 52

The present report describes the case of an intrauterine or early postnatal parvovirus infection with subsequent cerebellar hypoplasia in three kittens from the same litter. Clinical examination of affected cats revealed neurologic signs indicative of cerebellar ataxia. Due to poor prognosis, animals were euthanised and submitted for necropsy. Post mortem examination demonstrated variable degrees of cerebellar hypoplasia. Histologically, brain lesions were characterised by segmental loss of the external and internal granular layer and decreased numbers of Purkinje cells. Reactive proliferation of astrocytes in the central nervous system was verified by the detection of GFAP-expressing glial cells in affected areas using immunohistochemistry. Furthermore, parvovirus antigen was detected immunohistochemically in neuronal cells of the cerebellum, but not in other parts of the brain and spinal cord or non-neuronal tissues. The present report demonstrates the usefulness of post mortem examination and detection of viral antigen by immunohistochemistry for the discrimination of neurologic disorders in feline species. Neurologic deficiencies due to cerebellar hypoplasia caused by in utero or perinatal feline parvovirus infection should be taken into consideration as differential diagnoses for ataxia in neonatal and juvenile cats.
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PMID:Cerebellar hypoplasia in three sibling cats after intrauterine or early postnatal parvovirus infection. 1714 49

During a period of 1.5 months, a newly established pig herd experienced a high number of mummifications and stillbirths, a high neonatal mortality rate, and many piglets with congenital tremors or hind leg ataxia. After clinical and histological investigations, the submitted animals were divided into 4 groups: mummified or stillborn (N = 6), live born with myocarditis (N = 5) (average age 22.8 days), live born without myocarditis (N = 14) (average age 20.0 days), and control animals from a different herd (N = 5) (newborn). Statistically significant differences were observed in the mean porcine circovirus 2 (PCV2) load among the 4 groups in the liver (P < 0.0001). The presence of PCV2 antigen within the myocardial lesions was confirmed by immunohistochemistry. A high load of PCV2 DNA was observed in myocardium, liver, and spleen from mummified or stillborn piglets (>1 x 10(7) copies per 500 ng DNA), lower in piglets with myocarditis (>1 x 10(5) copies per 500 ng DNA), and even further lower in pigs without myocarditis (<1 x 10(5) copies per 500 ng DNA), whereas no PCV2 DNA was detected in the control animals. Myocardium, liver, and spleen were well suited for routine testing of fetuses and young piglets by quantitative real-time polymerase chain reaction. Neither porcine parvovirus nor encepaholomyocarditis virus was detected. These results indicate that the PCV2 infection might have been of etiological importance for the fetal deaths and piglet mortality observed in this herd.
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PMID:Association of myocarditis with high viral load of porcine circovirus type 2 in several tissues in cases of fetal death and high mortality in piglets. A case study. 1760 45

Human parvovirus B19 generally causes erythema infectiosum in childhood, but it can be associated with unusual findings, particularly in immunocompromised patients. This is a report about an immunocompetent 4-year-old female child affected with acute encephalitis by parvovirus B19, documented by polymerase chain reaction performed on cerebrospinal fluid, who was treated with intravenous immunoglobulins and dexamethasone and who developed a cerebellar syndrome with ataxia, dysmetria, and dysarthria. To the best of the authors' knowledge, this may be the first report of human parvovirus B19 encephalitis complicated by severe ataxia in childhood.
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PMID:Severe ataxia as a complication of human parvovirus B19 acute encephalitis in a child. 1848 17

We previously reported in a large cohort (N = 104) of post-mortem tissues the detection of both the non-pathogenic adeno-associated virus (AAV2) in approximately 13% and the pathogenic human parvovirus B19 (B19) in approximately 42% of human brains, particularly the dorsolateral prefrontal cortex. Multiple animal parvoviruses target the developing cerebellum (CBLM) resulting in hypoplasia and ataxia, but very little is known about the human parvoviruses and their ability to infect or cause disease in the CBLM. We have now confirmed in the above cohort the presence of AAV2 and B19 sequences in the CBLM. Our results show that approximately 27% and approximately 70% of human CBLM are positive by nested polymerase chain reaction for AAV2 and B19 sequences, respectively. We also document in a second cohort (N = 10) the presence of AAV2 (50%) and B19 (100%) sequences in the CBLM and correlate our results for B19 with studies from matched sera. Eighty percent (80%) of this cohort was positive for anti-B19 IgG, while none were IgM+, suggesting that most individuals had been previously infected with B19 but none acutely. To our knowledge, this study is the first to demonstrate that both AAV2 and B19 sequences are present at relatively high frequencies in the CBLM and are likely due to persistent rather than acute infection. Further studies will lead to insights into AAV2- and/or B19-CBLM interactions including mechanisms of infection, persistence, and possibly neuropathology, including cerebellar hypoplasia and ataxia.
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PMID:Persistent adeno-associated virus 2 and parvovirus B19 sequences in post-mortem human cerebellum. 1958 79


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