The Pathophysiology Tetanus

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Tetanus is an acute, often fatal disease caused by an exotoxin produced in a wound by Clostridium tetani. Clostridium tetani is a non-encapsulated, motile, anaerobic gram-positive bacillus obligatively. There are in vegetative and spore forms. Spores are very resistant to chemical disinfection or by heat, but the vegetative forms are susceptible to the bactericidal effect of heat, chemical disinfectants, and a number of antibiotics.

Clostridium tetani is a non-invasive body. It is found in soil and in the intestines and feces of horses, sheep, cattle, dogs, cats, rats, guinea pigs and chickens. Soil treated manure may contain many spores as well.

Tetanus occurs after spores or vegetative bacteria have access to tissues and produce toxins locally. The usual input mode is bowl a puncture wound or laceration. Tetanus can also follow elective surgery, burn wounds, otitis media, tooth infection, abortion and pregnancy. Neonatal tetanus usually follows an infection of the umbilical cord.

In the presence of anaerobic conditions, spores germinate. Toxins, including tetanolysin (which potentiates infection) and tetanospasmin (a potent neurotoxin) are produced. Tetanospasmin, often called tetanus toxoid, tetanus causes clinics. The toxin produced is distributed through the blood and lymphatic system. However, it does not penetrate the central nervous system in this way, because it can not cross the blood-brain barrier, except in the fourth ventricle. The toxin is occupied exclusively by the neuromuscular junction, where it migrates retrograde transynaptically to 75-250mm / day rate, a process that takes 3-14 days, free of neutralizing antitoxin, mainly in the inhibitory synapses to prevent acetylcholine release.

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 the sympathetic nervous system. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with the release of neurotrasmitters, blocking inhibitory impulses.

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

One of the many complications of tetanus is a secondary respiratory failure in spasm, obstruction by secretions, exhaustion and pulmonary aspiration. Cardiovascular complications appears to be due to hyperactivity of the sympathetic nervous system tachycardia, with heart rate over 180 beats per minute, severe vasoconstriction and hypertension. Dysautonomia is seen as increased activity and sympathy episodes of basal sympathetic activity. (SOA).

Wong Lai Teng

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