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Published on: October 2, 2014
Cerebrovascular damage in young rabbits after intravenous administration of Shiga toxin 2
M Mizuguchi1, J Sugatani, T Maeda
1Department of Pediatrics, Jichi Medical School, Tochigi, Japan. mmizuguc@ms.jichi.ac.jp
Insights
Young rabbits are more susceptible to Shiga toxin 2 (Stx2) than adults, developing severe central nervous system (CNS) vascular damage at lower doses. This study highlights age-dependent vulnerability to Shiga toxin-producing E. coli (STEC) neurotoxicity.
Area of Science:
- Neuroscience
- Toxicology
- Pediatrics
Background:
- Shiga toxin-producing Escherichia coli (STEC) causes acute encephalopathy, primarily in children.
- The age-dependent vulnerability of the central nervous system (CNS) to STEC toxins remains incompletely understood.
Purpose of the Study:
- To investigate the age-dependent vulnerability of the CNS to Shiga toxin 2 (Stx2).
- To compare the clinical and pathological effects of Stx2 on the CNS of young and adult rabbits.
Main Methods:
- Intravenous injection of Stx2 into young rabbits.
- Examination of clinical and pathological CNS effects.
- Comparison with adult rabbit responses.
Main Results:
- Neurological disorders were similar in young and adult rabbits, but lower Stx2 doses induced them in the young.
- Vascular lesions in the CNS of young rabbits appeared within 24 hours post-injection.
- Specific arteriolar changes, including endothelial hydropic swelling and medial cell karyorrhexis, were observed in young rabbits' CNS.
Conclusions:
- Immature cerebral blood vessels are more vulnerable to Stx2 than adult vessels in rabbits.
- The study suggests a heightened susceptibility of immature CNS vasculature to STEC-associated toxins.
Abstract:
Acute encephalopathy associated with Shiga toxin-producing Escherichia coli (STEC) primarily affects children. To elucidate the age-dependent vulnerability of the central nervous system (CNS), we injected Shiga toxin 2 (Stx2) intravenously to young rabbits and examined the clinical and pathological effects on the CNS. Although neurological disorders caused by Stx2 were similar between young and adult rabbits, the dose required to produce them in the young was one third of that required for the adults. Vascular lesions appeared as early as 24 h after injection in the young, but not at all in the adult. Arteriolar changes, such as hydropic swelling of the endothelial cells and karyorrhexis of the medial cells, were specific to the CNS of young animals. Evidence for apoptosis of vascular cells was scarce because DNA strand breaks and activation of caspases-3 and -9 were absent in the vast majority. Given our results, we conclude that the cerebral blood vessels of immature brains are more vulnerable to Stx2 than those of adults in the rabbit.
