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Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
Tetanospasmin (tetanus toxin) binds at the presynaptic terminals of lower motor neurons, causing peripheral neuromuscular failure (localized tetanus). The toxin is then carried by retrograde axonal transport to neurons in the spinal cord and brainstem, where toxin binds irreversibly. In the CNS, tetanus toxin enters the terminals of inhibitory (e.g. GABAergic) neurons. Synaptobrevin is degraded by the toxin, inhibiting the docking of vesicles containing neurotransmitters with the synaptic membrane, preventing neurotransmitter release. Tetanospasmin produces muscular rigidity by raising the resting firing rate of motor neurons via loss of inhibition, and generates spasms by failing to limit reflex responses to afferent stimuli. In the autonomic nervous system, a hypersympathetic state predominates, with a failure to inhibit the adrenal release of catecholamines. Toxin binding is a terminal and irreversible event. Recovery from tetanus appears to depend on the sprouting of a new axon terminal, which takes months.
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Tetanus and botulinum toxins alter synaptic transmission. A neurotoxic protein is produced in wounds contaminated by Clostridium tetani tetanospasmin, which when it reaches the central nervous system, results in tetanus. This condition represents an interference of inhibitory synaptic inputs on spinal motor neurons.474 Tetanospasmin causes functional disturbances of the balance between excitation and inhibition.578 The active toxin reaches the central nervous system by retrograde axonal transport. It is defected first within the perikaryon on motor neurons and causes tetanus when the toxin reaches the inhibitory synapses of the spinal cord.144 Clinical manifestations include muscle spasms, rigidity, and tetanic seizures.267
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Tetanus is typically a disease of soldiers, farmers, or gardeners. It is caused by deep penetrating wounds caused by objects contaminated with soil, which introduces spores into the tissue. As soon as the wound becomes anaerobic, the tetanus spores germinate to produce vegetative cells, which then multiply and release a potent neurotoxin called tetanospasmin. Only the tiniest quantities of exotoxin are required for the disease to develop. The bacteria producing the exotoxin are entirely non-invasive and lack all other virulence factors apart from the capacity to produce toxin. The exotoxin binds to local nerve endings, travels up the axon to the spinal cord, traverses a synaptic junction, and finally gains entry to the cytoplasm of inhibitory neurones. Within these cells the toxin exerts a highly specific proteolytic activity on one of the proteins (synaptobrevin) present in the vesicles that is responsible for the normal trafficking of inhibitory neurotransmitter to the synaptic junction. As a result, the inhibitory neurone cannot transmit its impulse and there is unopposed stimulation of skeletal muscles by motor neurones. Death is normally due to muscular spasm (spastic paralysis) extending to involve the muscles of the chest so that the patient is unable to breathe.
Suspected tetanus in an unvaccinated pediatric patient
Published in Baylor University Medical Center Proceedings, 2023
Kimberly Walter, Renita Thomas, Swasti Gyawali, Sowmya Kallur
Tetanus is a life-threatening vaccine-preventable illness. It is caused by tetanospasmin, a potent exotoxin of Clostridium tetani. Tetanospasmin causes neuromuscular dysfunction by inhibiting presynaptic GABA and glycine release. This leads to tonic spasms and paroxysmal contractions of skeletal muscles.1 Spores of Clostridium tetani are present throughout the environment in soil, dust, and manure and are often transmitted to humans via contaminated wounds. Tetanus is extremely rare in the United States due to vaccination efforts, with only 20 cases reported in 2018 and 26 cases in 2019.2,3 Here, we describe a suspected case of tetanus in a 10-year-old unvaccinated child in central Texas resulting in a 1-month stay in the pediatric intensive care unit and ultimately requiring a tracheostomy tube.
Intravenous magnesium sulphate infusion as first-line therapy in the control of spasms and muscular rigidity in childhood tetanus
Published in Paediatrics and International Child Health, 2019
Preeti Shanbag, Anupama Mauskar, Sanjeevani Masavkar
Tetanus is an acute, potentially fatal disease caused by Clostridium tetani. Cl. tetani spores enter the body either through a contaminated wound or through the ear in patients with chronic otitis media. Cl. tetani produces a neurotoxin, tetanospasmin, which affects both the central and peripheral nervous system. Gangliosides bind the toxin at the pre-synaptic nerve endings in the neuronal membrane, preventing the release of neurotransmitters (γ-aminobutyric acid—GABA and glycine). The resulting absence of inhibitory impulses manifests in the characteristic spasms and sympathetic over-activity seen in tetanus [1].
Dog bite injuries of the eye and ocular adnexa
Published in Orbit, 2019
Benjamin P. Erickson, Paula W. Feng, Sophie D. Liao, Yasha S. Modi, Audrey C. Ko, Wendy W. Lee
Tetanospasmin, the key pathogenic agent, is a zinc-dependent metalloproteinase consisting of two chains. The heavy chain binds to neuron cell surface receptors, while the light chain inhibits presynaptic neurotransmitter release.50 This degrades synaptobrevin in CNS inhibitory neurons, resulting in unchecked muscular contraction and hyperpyrexia.