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  • Updated 05.16.2020
  • Released 02.25.1994
  • Expires For CME 05.16.2023

Tetanus

Introduction

This article includes discussion of tetanus, cephalic tetanus, maternal tetanus, neonatal tetanus, and ophthalmoplegic tetanus. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Despite an effective immunization method, tetanus is still a threat in developing countries worldwide. In developed countries, this condition affects certain population groups, especially the elderly. In this article, the authors describe the clinical features of tetanus, which is characterized by sustained muscle rigidity and reflex spasm. Tetanospasmin, a toxin of Clostridium tetani, is responsible for these clinical symptoms. Besides symptomatic treatment, neutralization of this toxin is a mainstay for treating this condition. The beneficial effect of intrathecal immunoglobulin in conjunction with intramuscular administration has been proven in a randomized controlled clinical trial, and tetanus toxoid is considered very safe, even for immunodeficient individuals.

Key points

• Tetanus is caused by the neurotoxin tetanospasmin, produced by an anaerobic motile gram-positive rod, Clostridium tetani.

• This toxin interferes with the release of inhibitory neurotransmitter causing excessive excitation of spinal and bulbar motor neurons.

• The hallmarks of tetanus are sustained muscular rigidity and, in severe cases, reflex spasms.

• Autonomic instability, mostly hypersympathetic state, may occur in severe cases.

• Elimination of the source of toxin, toxin neutralization, control of muscle rigidity and spasms, and ventilatory support are the main strategies in treatment of tetanus.

Historical note and terminology

The earliest record of tetanus dates back to Egyptian civilization. It was demonstrated in case 7 in the Edwin Smith Surgical Papyrus, which involved a patient with trismus and nuchal rigidity after a penetrating skull injury (15). In 1890, a strychnine-like toxin, later known as tetanospasmin, was isolated from anaerobic soil bacteria and was proved to be responsible for clinical tetanus in experimental animals. Immunization with an inactivated derivative of this bacterial extract results in protection from clinical tetanus (54; 07).

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