Tetanus is due to:

# Tetanus is due to:
A. Exotoxin fixed to motor end plate
B. Endotoxin fixed to motor end plate
C. Circulating exotoxin
D. Circulating endotoxin

The correct answer is A. Exotoxin fixed to motor end plate.

Clostridium tetani produces two types of toxins:
 1. Endotoxin-cardiotoxin- selective on hemopoetic cells and cardiac tissue 
2. exotoxin; Tetanospasmin acts on acts at four sites
i). Motor end plate 
ii). Brain 
iii). spinal chord and 
iv) sympathetic nervous system. 

This Tetanospasmin inhibits cholinesterase at the motor end plate and as a result there is pooling of Acetyl choline resulting in sustained state of clonic muscle spasm, exotoxin travels to the CNS and it causes hyperexcitibity of the motor neurons at the Anterior horn cells there by evoking explosive spasms to sensory stimuli, once exotoxin is fixed in CNS, it cannot be neutralised by the antitoxin. 

C. tetani is an anaerobic, gram-positive, spore-forming rod whose spores are highly resilient and can survive readily in the environment throughout the world. Spores resist boiling and many disinfectants. In addition, C. tetani spores and bacilli survive in the intestinal systems of many animals, and fecal carriage is common. The spores or bacteria enter the body through abrasions, wounds, or (in the case of neonates) the umbilical stump. Once in a suitable anaerobic environment, the organisms grow, multiply, and release tetanus toxin, an exotoxin that enters the nervous system and causes disease. Very low concentrations of this highly potent toxin can result in tetanus (minimum lethal human dose, 2.5 ng/kg).

Genome sequencing of C. tetani has allowed identification of several exotoxins and virulence factors. Only those bacteria producing tetanus toxin ( tetanospasmin) can cause tetanus. Although closely related to the botulinum toxins in structure and mode of action, tetanus toxin undergoes retrograde transport into the central nervous system and thus produces clinical effects different from those caused by the botulinum toxins,  which remain at the neuromuscular junction.

Reference: S. Das Manual of Surgery and Harrison's Principles of Internal Medicine, 19th Edition, Page no: 984

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