By M. R. Popoff (auth.), Cesare Montecucco (eds.)
Tetanus has been recognized from the very starting of clinical literature because it was once first defined through Hyppocrates of Cos within the 5th century B.C. for twenty-four centuries it used to be thought of a neuro logical sickness till the step forward of CARLE and RATIONE (1884) who confirmed its infectious etiology. Following the institution of purified cultures of Clostridium tetani(KITASATO 1889), FABER (1890), and TIZZONI and CATIANI (1890) demon strated that the affliction is admittedly an intoxication because of a proteic neurotoxin. This toxin was once proven by way of BRUSHCHETIINI (1892) to maneuver retroaxonally and to behave on the spinal twine point. quickly thereafter VAN ERMENGEN (1897) tested that botu lism is additionally because of intoxication with a protein toxin produced by means of micro organism of the genus Clostridium. those micro organism and their spores and ubiquitous, and the vast majority of them don't produce neurotoxins. The selective good thing about generating such powerful toxin continues to be an issue of hypothesis (see Popoff, this volume). the following significant increase used to be the invention that tetanus neurotoxin 1 should be switched over by means of formaldehyde therapy to a nonpathogenic yet nonetheless absolutely immunogenic shape, and that this is often used effectively as a vaccine to avoid tetanus (RAMON and DESCOMBEY 1925). comparable vaccines (toxoids) should be ready with botulism neurotoxins (see MiDDLEBROOK and BROWN, this volume). The prevention oftetanus via vaccination (see Galatzka and Gasse, this quantity) is among the nice successes of simple learn coupled with a good public drugs service.
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Extra resources for Clostridial Neurotoxins: The Molecular Pathogenesis of Tetanus and Botulism
36 36 37 37 38 41 43 43 44 44 47 49 1 Introduction Tetanus has been known to mankind for thousands of years. The disease is ubiquitous, but it particularly kills many persons in tropical countries, where the disease is called by various local names (BYTCHENKO 1967). The belief that neonatal tetanus (NT) is linked with divine intervention is reflected in the Biblical story of the death of the son of King David and Bathsheba (2 Samuel, 11 and 12). World Health Organization, Expanded Programme on Immunization, 1211 Geneva, Switzerland 32 A.
Spores (ARNON 1989). Moderate to high toxin level (10-10 5 mouse lethal dose per gram) and viable C. botulinum are recovered from stools of affected infants for a long period after the onset of the symptoms, as long as 158 days. Toxin is seldom found in the serum of these patients. In foodborne botulism toxemia is common, and toxin usually disappears from the stools within several days and is rarely detectable in serum after 2 weeks. Infant botulism has been identified in many developed countries including Argentina, Australia, Canada, Chile, the former Czechoslovakia, United Kingdom, France, Italy, Japan, Spain, and Sweden, but most cases have been recorded in the United States (up to 90%), particularly in California.
N Engl J Med 315: 239-241 Considine RV, Simpson LL (1991) Cellular and molecular actions of binary toxins possessing ADPribosyltransferase activity. Toxicon 29: 913-936 Craig JM, Hayes S, Pilcher KS (1968) Incidence of Clostridium botulinum type E in salmon and other marine fish in the Pacific northwest. Appl Microbiol 16: 553-557 Creti R, Fenicia L, Aureli P (1990) Occurrence of Clostridium botulinum in the soil of the vicinity of Rome. Curr Microbiol 20: 317-321 Dezfulian M (1989) Animal models of botulism and tetanus.
Clostridial Neurotoxins: The Molecular Pathogenesis of Tetanus and Botulism by M. R. Popoff (auth.), Cesare Montecucco (eds.)