infectious diseases
Tetanus
Pathophysiology of Tetanus
C. tetanispores usually enter through contaminated wounds. Manifestations of tetanus are caused by an exotoxin (tetanospasmin) produced when bacteria lyse. The toxin enters peripheral nerve endings, binds there irreversibly, then travels retrograde along the axons and synapses, and ultimately enters the central nervous system (CNS). As a result, release of inhibitory transmitters from nerve terminals is blocked, thereby causing unopposed muscle stimulation by acetylcholine and generalized tonic spasticity, usually with superimposed intermittent tonic seizures. Disinhibition of autonomic neurons and loss of control of adrenal catecholamine release cause autonomic instability and a hypersympathetic state. Once bound, the toxin cannot be neutralized. Most often, tetanus is generalized, affecting skeletal muscles throughout the body. However, tetanus is sometimes localized to muscles near an entry wound. Tetanus toxin binds irreversibly to nerve terminals, and once bound, it cannot be neutralized. 