The most common source of a tetanus infection is through a puncture wound, and avoiding objects and environments that

put you at risk of these injuries will help you to avoid the disease. Even if you were able to completely eliminate the risk of puncture wounds, though,tetanus bacteria can enter the body through other types of injuries, such as cuts, burns or insect bites. The only truly effective method of preventing tetanus infection is through inoculation. Tetanus bacteria might be present nearly anywhere but are most commonly found in soil, manure and dust. While in these environments, tetanus exists as a spore, remaining dormant until introduced to a host. After they are in the body, the spores activate, and the bacteria begin producing powerful toxins. Within a few weeks, or sometimes as quickly as four days, symptoms become apparent. Patients might experience fever, sweating, diarrhea or bloody stools, headache, sore throat and an accelerated heartbeat, but the primary indicator of tetanus is muscle spasming. This begins as stiffness in the jaw, and muscle spasms eventually cause the jaw to clench tight. It is for this reason that the tetanus infection is sometimes referred to as lockjaw.
Ultimately, this produces the symptoms of the disease. Damaged upper motor neurons can no longer inhibit lower motor neurons, plus they cannot control reflex responses to afferent sensory stimuli.

Tetanus begins when spores of ''Clostridium tetani'' enter damaged tissue. The spores transform into rod-shaped bacteria and produce the neurotoxin tetanospasmin (also known as tetanus toxin). This toxin is inactive inside the bacteria, but when the bacteria dies, it is released and activated by proteases. Active tetanospasmin is carried by retrograde axonal transport to the spinal cord and brain stem where it binds irreversibly to receptors at these sites. which in turn blocks neurotransmission. Ultimately, this produces the symptoms of the disease. Damaged upper motor neurons can no longer inhibit lower motor neurons, plus they cannot control reflex responses to afferent sensory stimuli.

The clinical triad consists of muscle rigidity, spasms and autonomic dysfunction. Early symptoms are neck stiffness, sore throat and poor mouth opening.

called opisthotonus. Gastric stasis. blocking release of inhibitory transmitter from nerve terminals and thereby causing a generalized tonic spasticity. Spasms may be spontaneous or triggered by visual. Most often. usually with superimposed intermittent tonic seizures. This results in tachycardia. Other features include excessive salivation and sweating (may lead to dehydration). with basal catecholamine levels rising ten-fold. diarrhea and high output renal failure may also be related to the autonomic disturbance. Tetanospasmin binds irreversibly to the ganglioside membranes of nerve synapses. ileus. Poor cough. .Increased muscle tone may affect agonist and antagonist muscle groups together. tetanus is generalized. resembling a convulsion. Respiratory failure continues to be a major cause of mortality in developing countries. Autonomic dysfunction results from paroxysmal increases in sympathetic activity. tetanus is sometimes localized to muscles near an entry wound. Pharyngeal and laryngeal spasms may lead to aspiration or airway obstruction. Muscles of the head and neck are usually affected first. with muscles throughout the body affected. Neck stiffness and dysphagia are also common. Disinhibition of autonomic neurons and loss of control of adrenal catecholamine release cause autonomic instability and a hypersympathetic state. with a hyperkinetic circulation. whereas severe autonomic dysfunction causes most deaths in the developed world. Continual spasms may lead to respiratory failure. giving rise to masseter spasm (trismus or ‘lockjaw’) and a typical facial expression (risus sardonicus). Pathophysiology Manifestations of tetanus are caused by an exotoxin (tetanospasmin). The effects on the parasympathetic system are less clear. The toxin may enter the CNS along the peripheral motor nerves or may be bloodborne to nervous tissue. inability to swallow. low/normal systemic vascular resistance and normal right and left sided cardiac filling pressures. cardiomyopathy and myocardial infarction. Once bound. hypertension and pyrexia. However. The most common form of tetanus (80 %) is generalized tetanus. affecting skeletal muscles throughout the body. gastric stasis all increase the risk of aspiration. the toxin cannot be neutralized. auditory or emotional stimuli and can be severe enough to cause fractures or avulse tendons. Truncal rigidity with predominant extensor spasm may lead severe arching of the back during spasm.

Respiratory failure is the most common cause of death. and the autonomic nervous system may also be affected. diaphragm. The typical clinical manifestations of tetanus are caused when tetanus toxin interferes with release of neurotransmitters.Spasms: Facial muscle spasm produces a characteristic expression with a fixed smile and elevated eyebrows (risus sardonicus). Hypoxemia can also induce cardiac arrest. During generalized spasms. generalized tonic spasms with profuse sweating are precipitated by minor disturbances such as a draft. Sphincter spasm causes urinary retention or constipation. spinal cord. Protracted tetanus may manifest as a very labile and overactive sympathetic nervous system. including periods of hypertension. tachycardia. This leads to unopposed muscle contraction and spasm. and in the sympathetic nervous system. neck. or movement. Seizures may occur. and chest wall muscles cause asphyxiation. Dysphagia may interfere with nutrition. is present. Autonomic instability: Temperature is only moderately elevated unless a complicating infection. Rigidity or spasm of abdominal. noise. Laryngeal spasm and rigidity and spasms of the abdominal wall. such as pneumonia. Mental status is usually clear. Respiratory and pulse rates are increased. and back muscles—even opisthotonos—may occur. tetani usually enters the body through a wound. but coma may follow repeated spasms. causing cyanosis or fatal asphyxia. Spasms also interfere with respiration. contributing to a hypoxemic death. Toxins act at several sites within the central nervous system. and brain. Reflexes are often exaggerated. the spores germinate. patients are unable to speak or cry out because of chest wall rigidity or glottal spasm. Characteristic painful. and myocardial irritability. . Toxins are produced and disseminated via blood and lymphatics. including peripheral motor end plates. and pharyngeal spasm leads to aspiration of oral secretions with subsequent pneumonia. Pathogenesis C. In the presence of anaerobic (low oxygen) conditions. The immediate cause of death may not be apparent. blocking inhibitor impulses.

and are spread by animal and human feces. . particularly a puncture wound. physiological TETANUS. more often. a highly fatal disease caused by the bacillus Clostridium tetani. characterized by muscle spasms and convulsions. and seizures. The bacilli are prevalent in rural areas and grow in the intestines of humans and other animals. They are found in soil and dust. which typically infe cts the bodythrough a deep wound. often fatal disease that is characterized byspasmodic contracti on of voluntary muscles. there is obvious infection. A state of continuous muscular contraction. Tetanus toxin can affect neonates to cause muscle spasms. which causes the muscles to tighten up in a continuous ("tetanic" or "tonic") contraction or spasm. such as one caused by a nail. splinter. an d that is caused by theneurotoxin Clostridium tetani. especially wheninduced artif icially by rapidly repeated stimuli. Occasionally. or gunshot. 1. 2. Definition Tetanus is a rare but often fatal disease that affects the central nervous system by causing painful muscular contractions. Because of the characteristic jaw stiffness. It begins when tetanus bacteria enter the body. especially oneoccurring in the neck and jaw. 2. inability to nurse. tetanus [tet´ah-nus] 1.How does the tetanus toxin cause damage to the body? The tetanus toxin affects the site of interaction between the nerve and the muscle that it stimulates. The tetanus toxin amplifies the chemical signal from the nerve to the muscle. This results in either localized or generalized muscle spasms. Also called lockjaw . insect bite. usually through a wound or cut exposed to contaminated soil. it is also known as lockjaw. entering the body through a break in the skin. This region is called the neuromuscular junction. An acute. the original wound appears trivial and heals quickly.

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