Read in | English | Español | Français | Deutsch | Português | Italiano | 日本語 | 한국어 | 简体中文 | 繁體中文 | العربية | Dansk | Nederlands | Filipino | Finnish | Ελληνικά | עִבְרִית | हिन्दी | Bahasa | Norsk | Русский | Svenska | Magyar | Polski | Română | Türkçe

Tetanus Pathophysiology

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.

Further Reading


This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Tetanus" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc.