Disease
C. tetani causes tetanus
Transmission
Spores are widespread in soil. The portal of entry is usually a wound site (e.g., where a nail penetrates the foot), but the spores can also be introduced during “skin-popping,” a technique used by drug addicts to inject drugs into the skin. Germination of spores is favored by necrotic tissue and poor blood supply in the wound. Neonatal tetanus, in which the organism enters through a contaminated umbilicus or circumcision wound, is a major problem in some developing countries.
Pathogenesis
Tetanus toxin (tetanospasmin) is an exotoxin produced by vegetative cells at the wound site, not by the spores. This polypeptide toxin is carried intra-axonally (retrograde) to the central nervous system, where it binds to ganglioside receptors and blocks the release of inhibitory mediators (e.g., glycine and γ-aminobutyric acid [GABA]) at spinal synapses. Tetanus toxin is encoded by a plasmid, unlike botulinum toxin which is encoded by a lysogenic bacteriophage.
Tetanus toxin and botulinum toxin (see later) are among the most toxic substances known. They are both proteases that cleave the proteins involved in mediator release from the neurons.
Tetanus toxin has one antigenic type, unlike botulinum toxin, which has eight. There is therefore only one antigenic type of tetanus toxoid in the vaccine against tetanus.
Clinical Findings
Tetanus is characterized by strong muscle spasms (spastic paralysis, tetany). Specific clinical features include lockjaw (trismus) due to rigid contraction of the jaw muscles, which prevents the mouth from opening; a characteristic grimace known as risus sardonicus; and exaggerated reflexes. Opisthotonos, a pronounced arching of the back due to spasm of the strong extensor muscles of the back, is often seen. Respiratory failure ensues. A high-mortality rate is associated with this disease. Note that in tetanus, spastic paralysis (strong muscle contractions) occurs, whereas in botulism, flaccid paralysis (weak or absent muscle contractions) occurs.
Laboratory Diagnosis
There is no microbiologic or serologic diagnosis. Organisms are rarely isolated from the wound site. C. tetani produces a terminal spore (i.e., a spore at the end of the rod). This gives the organism the characteristic appearance of a “tennis racket.”
Treatment
Tetanus immune globulin (tetanus antitoxin) is used to neutralize the toxin. The role of antibiotics is uncertain. If antibiotics are used, either metronidazole or penicillin G can be given. An adequate airway must be maintained and respiratory support given. Benzodiazepines are given to prevent spasms.
Prevention
Tetanus is prevented by immunization with tetanus toxoid (form aldehyde-treated toxin) in childhood and every 10 years thereafter. Tetanus toxoid is usually given to children in combination with diphtheria toxoid and the acellular pertussis vaccine (DTaP).
When trauma occurs, the wound should be cleaned and debrided, and tetanus toxoid booster should be given. If the wound is grossly contaminated, tetanus immune globulin, as well as the toxoid booster, should be given and penicillin administered. Half of the immune globulins should be infiltrated into the wound and the other half given intramuscularly at a site separate from the tetanus toxoid.
Tetanus immune globulin (tetanus antitoxin) is made in humans to avoid serum sickness reactions that occur when antitoxin made in horses is used. The administration of both immune globulins and tetanus toxoid (at different sites in the body) is an example of passive–active immunity.
