The Pathophysiology of Tetanus

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The Pathophysiology of Tetanus

Tetanus is an acute, often fatal disease caused by an exotoxin produced in a wound by Clostridium tetani. Clostridium tetani is a gram-positive, nonencapsulated, motile, obligatively anaerobic bacillus. It exists in vegetative and sporulated forms. Spores are highly resistant to disinfections by chemical or heat, but vegetative forms are susceptible to the bactericidal effect of heat, chemical disinfectants, and a number of antibiotics.

Clostridium tetani is a noninvasive organism. It is found in soil and in the intestine and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs and chicken. Manure-treated soil may contain large numbers of spores too.

Tetanus occurs after spores or vegetative bacteria gain access to tissues and produce toxin locally. The usual mode of entry is trough a puncture wound or laceration. Tetanus may also follow elective surgery, burn wounds, otitis media, dental infection, abortion and pregnancy. Neonatal tetanus usually follows infection of the umbilical stump.

In the presence of anaerobic conditions, the spores germinate. Toxins,including tetanolysin (which potentiates infection) and tetanospasmin (a potent neurotoxin) are produced. Tetanospasmin, often referred to as tetanus toxin, causes clinical tetanus. The toxin produced is disseminated through the bloodstream and lymphatic system. However, it does not enter the central nervous system through this route, as it cannot cross the blood brain barrier except at the fourth ventricle. The toxin is exclusively taken up by

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the neuromuscular junction, where it migrates retrograde transynaptically at the rate 75-250mm/day, a process which takes 3-14 days, protected from neutralizing antitoxin, predominantly to inhibitory synapses to prevent the release of acetylcholine.

The toxin acts after the incubation period (3-14) days) at several sites within the central nervous system, including peripheral motor end plates, spinal cord, brain and sympathetic nervous system. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with release of neurotrasmitters, blocking inhibitor impulses.

Blockade of spinal inhibition is produced when the toxin acts at the synapse of interneurons of inhibitory pathways and motor neurons. General muscle rigidity arises from uninhibited afferent stimuli entering the central nervous system from the periphery. The effect of the toxin on the brain is controversial; direct inoculation can cause seizures.

One of the many complications from tetanus is respiratory failure secondary to spasms, obstruction by secretions, exhaustion and pulmonary aspiration. Cardiovascular complications thought to be due to hyperactivity of the sympathetic nervous system include tachycardia, with heart rates over 180 beats per minute, severe vasoconstriction and hypertension. Autonomic dysfunction is seen as increased basal sympathetic activity and episodes of sympathetic over activity. (SOA).

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