Virological markers in cerebrospinal fluid are predictive of ovine lentivirus-associated subclinical encephalomyelitis

Brodie, Scott J.; Bickle, Heidi M.; DeMartini, James C.

doi:10.1016/0090-1229(95)90131-0

Cited by 10 publications

(2 citation statements)

References 24 publications

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“…Ependyma and CP in all four ventricles become diffusely necrotic (Bourgouin et al 1992). Another infection of CP-CSF is by ovine lentivirus, which invades periventricular sites as part of a more generalized encephalomyelitis (Brodie, Bickle, and DeMartini 1995); the CSF lentiviral markers reflect CNS pathology. Various blood cells have greatly restricted access to CSF except in pathophysiologic conditions associated with autoimmune disease or hemorrhage into CP-ependymal zones.…”

Section: Periventricular Lesions and The Choroid Plexus-csf Nexusmentioning

confidence: 99%

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

et al. 2010

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Bordering the ventricular cerebrospinal fluid (CSF) are epithelial cells of choroid plexus (CP), ependyma and circumventricular organs (CVOs) that contain homeostatic transporters for mediating secretion/reabsorption. The distributional pathway (''nexus'') of CP-CSF-ependyma-brain furnishes peptides, hormones, and micronutrients to periventricular regions. In disease/toxicity, this nexus becomes a conduit for infectious and xenobiotic agents. The sleeping sickness trypanosome (a protozoan) disrupts CP and downstream CSF-brain. Piperamide is anti-trypanosomic but distorts CP epithelial ultrastructure by engendering hydropic vacuoles; this reflects phospholipidosis and altered lysosomal metabolism. CP swelling by vacuolation may occlude CSF flow. Toxic drug tools delineate injuries to choroidal compartments: cyclophosphamide (vasculature), methylcellulose (interstitium), and piperazine (epithelium). Structurally perturbed CP allows solutes to penetrate the ventricles. There, CSF-borne pathogens and xenobiotics may permeate the ependyma to harm neurogenic stem cell niches. Amoscanate, an anti-helmintic, potently injures rodent ependyma. Ependymal/brain regions near CP are vulnerable to CSF-borne toxicants; this proximity factor links regional barrier breakdown to nearby periventricular pathology. Diverse diseases (e.g., African sleeping sickness, multiple sclerosis) take early root in choroidal, circumventricular, or perivascular loci. Toxicokinetics informs on pathogen, anti-parasitic agent, and auto-antibody distribution along the CSF nexus. CVOs are susceptible to plasma-borne toxicants/pathogens. Countering the physico-chemical and pathogenic insults to the homeostasis-mediating ventricle-bordering cells sustains brain health and fluid balance.

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Section: Periventricular Lesions and The Choroid Plexus-csf Nexusmentioning

confidence: 99%

The Distributional Nexus of Choroid Plexus to Cerebrospinal Fluid, Ependyma and Brain

et al. 2010

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“…Clinical cases of Maedi are distributedall over the world (21); however, there arereports from severalcountries about the serological prevalenceofantibodies againstMVV in sheep without manifest clinical signs (3,7,16). Alot of experimentalwork hasbeen done on the pulmonary as well as on the neurological formofthe disease (4,8,13,15,20,30,31).…”

Section: Introductionmentioning

confidence: 99%

Clinic and CNS pathology of natural Visna cases

Ganter¹,

Henze²,

Wohlsein³

2007

Tierarztl Prax Ausg G

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Summary Objective: This study summarizes the clinical, serological, pathomorphological and laboratory findings in 19 sheep with spontaneous Visna in Germany. The cases occurred over a period of 13 years in 13 flocks. In all affected sheep cytologic examination of cerebrospinal fluid (CSF) was performed. In addition in six flocks from which 12 of the Visna cases came the whole flock was tested for Maedi/Visna virus (MVV) antibodies. Material and methods: The diagnosis of spontaneous Visna with typical clinical signs was proven by serological and histopathological investigations. Serological screening for MVV antibodies was performed with the agargel-immuno- precipitation-test (AGIDT). Additionally, cerebrospinal fluid (CSF) was obtained by lumbosacral puncture and examined cytologically. Results: Nine of the 19 cases were Texels and six East Frisian Milk sheep. Six out of nine Texels came from the same flock with a MVV-antibody intra-flock prevalence of 0.94. The mean age of the sheep was 3.9 ± 2.3 years (0.5–10 years). Time between onset of clinical symptoms until euthanasia due to recumbency was 35 ± 23 days (6–102 days). In most cases clinical signs started with ataxia, staggering and circling, followed by increasing paresis of the hind legs. In the late stages of the disease 14 sheep suffered from tetraparesis. Trembling of lips or eye lids, blindness and scratching were rare signs. In all cases pleocytosis (11–876 M/l, mean = 167 M/l) with mononuclear cells, predominantly macrophages, was found. This finding provides an additional diagnostic aid to support the clinical differentiation from other infectious diseases with neurological manifestation in sheep. Histopathology of the CNS revealed in most cases a severe leukoencephalitis and demyelinisation with perivascular lymphocytic infiltration. Conclusion and clinical relevance: Visna is an important differential diagnosis in CNS disorders of sheep. It also occurs in animals younger than one year. Visna occurs especially in highly infected flocks of susceptible sheep breeds. CSF cytology can help to differentiate Visna from other CNS diseases. Clinically, Visna may be an important differential diagnosis to Scrapie.

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