Blood changes and post‐mortem findings following intravenous inoculation of sheep with culture filtrates of <i>Cl. welchii</i>, types A, C and D

Gordon, W. S.; Stewart, James; Holman, H.H.; Taylor, A. Wilson

doi:10.1002/path.1700500207

Cited by 19 publications

(5 citation statements)

References 7 publications

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“…Epsilon toxin is a major virulence determinant of Clostridium perfringens types B and D, which cause fetal enterotoxemia of domestic animals [1]. Neurologic features, such as tremor and opisthotonus, which are characteristically observed during the course of the enterotoxemia [2], can be induced by epsilon intoxication in experimental models [3,4]. The toxin accumulates mainly in the brain and a high‐affinity binding site for epsilon toxin exists in the synaptosomal membrane [5,6].…”

Section: Introductionmentioning

confidence: 99%

Clostridium perfringensepsilon toxin causes excessive release of glutamate in the mouse hippocampus

Miyamoto

Sumitani

Nakamura

et al. 2000

FEMS Microbiology Letters

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The mechanism of neurotoxicity of Clostridium perfringens epsilon toxin to the mouse brain was investigated. Intravenous injection in mice with the toxin caused seizure and excited hippocampal neurons. Microdialysis revealed that epsilon toxin induced excessive glutamate release in the hippocampus. Both the seizure and glutamate release were attenuated by prior injection with riluzole, an inhibitor of pre-synaptic glutamate release, suggesting that this toxin enhances glutamate efflux, leading to seizure and hippocampal neuronal damage.

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Section: Introductionmentioning

confidence: 99%

Clostridium perfringensepsilon toxin causes excessive release of glutamate in the mouse hippocampus

Miyamoto

Sumitani

Nakamura

et al. 2000

FEMS Microbiology Letters

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“…Characteristic neurologic features have also been reported for an experimental animal model: muscular incoordination, tremor, and pleurothotonos developed after the toxin was injected intravenously (i.v.) into a mouse (15). Pathological changes caused by the toxin were observed mainly in the brain (10,14).…”

mentioning

confidence: 99%

Neurotoxicity of Clostridium perfringens Epsilon-Toxin for the Rat Hippocampus via the Glutamatergic System

Miyamoto¹,

Minami²,

Toyoshima³

et al. 1998

Infect Immun

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The neurotoxicity of epsilon-toxin, one of the major lethal toxins produced by Clostridium perfringens type B, was studied by histological examination of the rat brain. When the toxin was injected intravenously at a lethal dose (100 ng/kg), neuronal damage was observed in many areas of the brain. Injection of the toxin at a sublethal dose (50 ng/kg) caused neuronal damage predominantly in the hippocampus: pyramidal cells in the hippocampus showed marked shrinkage and karyopyknosis, or so-called dark cells. The dark cells lost the immunoreactivity to microtubule-associated protein-2, a postsynaptic somal and dendric marker, while acetylcholinesterase-positive fibers were not affected. Timm’s zinc staining revealed that zinc ions were depleted in the mossy layers of the CA3 subfield containing glutamate as a synaptic transmitter. The cerebral blood flow in the hippocampus was not altered significantly before or after administration of the toxin, as measured by laser-Doppler flowmetry, excluding the possibility that the observed histological change was due to a secondary effect of ischemia in the hippocampus. Prior injection of either a glutamate release inhibitor or a glutamate receptor antagonist protected the hippocampus from the neuronal damage caused by epsilon-toxin. These results suggest that epsilon-toxin acts on the glutamatergic system and evokes excessive release of glutamate, leading to neuronal damage.

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“…Neurologic features, such as tremor and opisthotonus, which are characteristically observed during the course of the enterotoxemia [2], can be induced by epsilon intoxication in experimental models [3,4]. The toxin accumulates mainly in the brain and a high-a¤nity binding site for epsilon toxin exists in the synaptosomal membrane [5,6].…”

Section: Introductionmentioning

confidence: 99%

Clostridium perfringens epsilon toxin causes excessive release of glutamate in the mouse hippocampus

Miyamoto

2000

FEMS Microbiology Letters

View full text Add to dashboard Cite

The mechanism of neurotoxicity of Clostridium perfringens epsilon toxin to the mouse brain was investigated. Intravenous injection in mice with the toxin caused seizure and excited hippocampal neurons. Microdialysis revealed that epsilon toxin induced excessive glutamate release in the hippocampus. Both the seizure and glutamate release were attenuated by prior injection with riluzole, an inhibitor of presynaptic glutamate release, suggesting that this toxin enhances glutamate efflux, leading to seizure and hippocampal neuronal damage. ß

show abstract

Blood changes and post‐mortem findings following intravenous inoculation of sheep with culture filtrates of Cl. welchii, types A, C and D

Cited by 19 publications

References 7 publications

Clostridium perfringensepsilon toxin causes excessive release of glutamate in the mouse hippocampus

Clostridium perfringensepsilon toxin causes excessive release of glutamate in the mouse hippocampus

Neurotoxicity of Clostridium perfringens Epsilon-Toxin for the Rat Hippocampus via the Glutamatergic System

Clostridium perfringens epsilon toxin causes excessive release of glutamate in the mouse hippocampus

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