MM 299-302; ID 1175-1185
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NAME OF DISEASE:     Tetanus

ETIOLOGICAL AGENT:     Clostridium tetani


    The disease usually begins as an infection resulting from trauma. Suspect tetanus in cases involving:

    1.     Drug addicts

    2.     Animal bites

    3.     Deep wounds

    4.     Home births

    During trauma, the spores of C. tetani, which are ubiquitous in dust, are injected into the tissue along with other organisms. The aerobic organisms grow initially until the redox potential of the tissue is low. This allows the germination of the clostridial spores and a localized infection results. Proliferating cells elaborate a toxin, tetanospasmin, which causes a systemic toxemia.


    The tetanospasmin spreads from the infected site to the CNS by two mechanisms:

    1.     Adsorption at myoneural junctions followed by migration through perineural tissue spaces of
            nerve trunks to the CNS.

    2.     Passage from tissue spaces to lymphatics, to blood, to the CNS.

    Regardless of the route, the toxin becomes bound to gangliosides in the CNS.

    The time consumed in the passage represents the larger part of the incubation period of 2-50 days. This toxin is one of the most potent poisons known. The physiological action is identical to that of strychnine. Both substances suppress inhibiting influences on the motor neurons and interneurons without directly enhancing synaptic excitory action. The toxin also affects synaptic transmission at myoneural junctions. There are no lesions formed in the CNS.


    Clues to the diagnosis of tetanus are:

    1.     A wound or recent history of a wound

    2.     No clear history of tetanus toxoid immunization

    3.     Irritability

    4.     Restlessness

    5.     Headache

    6.     Low grade fever or no fever

    Two basic forms of tetanus may be distinguished: local and general. Local tetanus consists of spasm and increased muscle tone confined to muscles near the wound; there are no systemic signs. General tetanus is far more frequent. Almost all neonatal tetanus is the general form. The first sign is difficulty in sucking, beginning 8-10 days after birth and progressing to total inability to suck.

    The most characteristic complaint of adult patients with general tetanus is lockjaw or trismus, the inability to open the mouth because of spasm of the masseter muscles. Spasm of the facial muscles leads to a grotesque grinning expression termed risus sardonicus. Spasms of the somatic musculature in general tetanus may be widespread, resulting in opisthotonos (a form of spasm in which the head and the heels are bent backward and the body bowed forward) and boardlike rigidity of the abdomen. Acute, paroxysmal incoordinate widespread spasms of the muscles are characteristic of moderate and severe tetanus. Such tonic convulsions occur intermittently, irregularly and unpredictably, persisting for a few seconds to several minutes. Initially mild and separated by periods of relaxation, paroxysms tend to become more painful, severe and exhausting as they continue. Paroxysms may occur spontaneously or may be precipitated by a variety of external stimuli such as:

    1.     Drafts of cold air

    2.     Noise

    3.     Turning on lights

    4.     Attempt of patient to drink

A physical examination will reveal:

    1.     Trismus

    2.     Hypertonicity of muscles

    3.     Hyperactive deep tendon reflexes

    4.     Clean mentation

    5.     Local or general muscle spasms

Laboratory examination will reveal:

    1.     Moderate leukocytosis

    2.     Normal CSF

    3.     Presence of C. tetani in wounds (in 1/3 of patients)

    4.     Normal serum calcium


    1.     Dental abscess (results in stiff jaw) - differentiate via x-ray.

    2.     Meningitis - examination of CSF.

    3.     Encephalitis is occasionally associated with trismus and muscle spasms but sensorium of
            such patients is clouded.

    4.     Rabies - trismus is not present, usually incubation period is longer. Spinal fluid may be
            pleocytotic (larger than normal number of cells).

    5.     Strychnine poisoning - low serum calcium, trismus appears late.


    The quality of the supportive care determines the prognosis. Overall case fatality rate is 60% but is only 10% in centers where it is common. Poorest prognosis is in very young and very old. Death is usually due to asphyxiation.


    The objectives of treatment are:

    1     To provide supportive care until the toxin that attaches to gangliosides is metabolized.

            a.     Treat with muscle relaxants

                    (1)     Curare

                    (2)     Diazepam

            b.     Connect to a respirator

            c.     Avoid external stimuli that may trigger spasms.

    2.     To neutralize circulating toxin. Inject tetanal immune globulin (TIG) of human origin IM at
            three sites. TIG neutralizes circulating toxin but does not pass the blood-brain barrier and
            thus has no effect on bound toxin. Actively immunize with toxoid.

    3.     To remove the source of tetanospasmin - debride the wound, irrigate with 3% hydrogen
            peroxide. Administer large dose of penicillin G/or alternately tetracycline. This may do little
            good since the organism only grows in areas where there is a poor blood supply.


    Administer DTP (diphtheria, tetanus, pertussis) vaccine at 2, 4, 6, and 15 months and 4-6 years of age. Give tetanus and diphtheria toxoid at 14-16 years of age and repeat every 10 years throughout life.

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