Chapter 35

### INTRODUCTION

Tetanus is an infectious disease caused by the neurotoxin of the anaerobic, gram-negative bacillus Clostridium tetani. In developed countries it is rare due to vaccination programs. Clostridium tetani produces two exotoxins: tetanolysin and tetanospasmin. The latter is responsible for the clinical manifestations of the tetanus disease.

### PATHOPHYSIOLOGY

Clostridium tetani spores enter tissues through a contaminated wound where they incubate and release tetanospasmin. This toxin has a preference for inhibitory neurons and spreads by first entering local peripheral neurons, where it is internalized. It is then transported intra-axonally and retrograde to the cell body. Once the toxin reaches the CNS, it binds to gangliosides at the presynaptic inhibitory nerves and blocks the release of inhibitory neurotransmitters.

The mechanism of action of this toxin is mostly at the presynaptic membrane where it degrades synaptobrevin, a protein involved in the fusion of neurotransmitter vesicles to nerve membranes. As a result, fusion is inhibited and neurotransmitters are not released into the synapse.

In the spinal cord, this toxin suppresses alpha motor neurons, resulting in generalized skeletal muscle contractions or spasms. In the brain, the toxin interrupts the release of gamma-amino butyric acid (GABA) and glycinergic neurons. Autonomic dysfunction with sympathetic nervous system hyperactivity occurs with disease progression.

### SIGNS AND SYMPTOMS

Diagnosis of tetanus is clinical and suspected after a history of an open, contaminated wound. Differential diagnosis includes drug-induced dystonia, neuroleptic malignant syndrome, hypocalcemia, strychnine poisoning, sepsis, and encephalitis. The disease commonly presents after an incubation period during which patients complain of dysphagia, neck stiffness, and jaw stiffness. The muscles of the head and neck are usually affected first with progressive spread to the rest of the body. As the disease progresses, rigidity and trismus occur. Trismus is the presenting symptom in most patients due to masseter muscle spasms.

Patients can present with ventilatory impairment that follows a restrictive disease pattern due to intercostal and diaphragm spasms. Laryngospasm and dysphagia may occur due to laryngeal and pharyngeal muscle spasm, respectively. As disease progresses, abdominal and lumbar muscles become rigid and account for the characteristic opisthonic posture. Patients may complain of severe pain secondary to tonic-clonic skeletal muscle spasms and present with an elevated body temperature due to the increased skeletal muscle work. The severity of the spasms can lead to rhabdomyolysis.

Autonomic dysfunction is a progressive manifestation that presents as tachycardia, blood pressure lability, and cardiac arrhythmias. Profuse salivation and increased bronchial secretions are among other side effects. Patients can also present with diaphoresis, intense peripheral vasoconstriction, and increased urinary excretion of cathecholamines (secondary to sympathetic system overactivity).

### TREATMENT

If the immunization status is unknown, administration of human tetanus immunoglobulin, immunization, and antibiotics are required. Intramuscular human immunoglobulin will neutralize circulating toxins and will prevent neurotoxin entry to neurons; it will not ...

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