Rapid death of infant rhesus monkeys injected with Clostridium difficile toxins A and B: Physiologic and pathologic basis2
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Are Clostridium difficile toxins nephrotoxic?
2019, Medical HypothesesCitation Excerpt :Post-mortem tissue has been available from both experimental animal models and human deaths. Infant monkeys were exposed to C. difficile toxin either through the intravenous or intraperitoneal routes, and they suffered demise [60]. Both toxin A and B exposures were associated with increases in serum creatinine up until the time of animal death, but the peak levels were relatively low even though a 100–200% change in values was determinable.
Severe Nervous System Complications After Botulinum Type A Therapy: Three Case Reports With Reviews of FDA-Reported Nervous System Adverse Effects
2012, PM and RCitation Excerpt :Cowdry and Nickolson concluded that, in humans, secondary causes such as pneumonia or the consequences of hypoxia were likely and were mistakenly reported as a primary etiology of death [35]. Death attributable to other toxins in the clostridium family showed similar pathology results [38], suggesting that unless SNAP-25 enzyme activity is specifically investigated in patients who died after receiving BoNT/A, a causal relationship to the toxin may not be established. This scenario is not surprising because botulinum causes neuronal and cell-to-cell communication failure, impairing the function of the organism as a whole rather than killing singular cells [36,39].
Immunological evidence for a bacterial toxin aetiology in sudden infant death syndrome
1999, FEMS Immunology and Medical MicrobiologyCan superantigens trigger sudden infant death?
1994, Medical HypothesesThe role of infectious agents in sudden infant death syndrome
1994, FEMS Immunology and Medical Microbiology
- 2
Presented in part at the 82nd Annual Meeting of the American Society for Microbiology, Atlanta, March 11, 1982.
- 1
From the California Department of Health Services: the California Primate Research Center, University of California, Davis; and the Virginia Polytechnic Institute and State University.
Supported by a grant from the Henry J. Kaiser Family Foundation, the National Institutes of Health (grants HD-14548, HD-12530, AI-16354, AI-15749, and RR-00169), the California Department of Health Services, and the Commonwealth of Virginia.