Ans. b (Soil). (Ref. Ananthanarayan, Microbiology, 4th/pg.245)TETANUS# Caused by Clostridium tetani# Seen following deep or penetrating wound in relatively avascular areas# More prevalent in developing countries# Seen in neonate (tetanus neonaturum) following the use of cow dung on the umbilicus# Microbiology- Gram-positive spore forming rod (Clostridium tetani is a gram-positive anaerobic bacillus)- Typical 'drum-stick' appearance with terminal spore- Widely found in the environment and soil- A Strict anaerobe that produces a powerful exotoxin- The neurotoxin is a powerful exotoxin- Exotoxin is resistant to autoclaving- Exotoxin is not antigenic and repeat infection can occur- Infection produces few signs of local inflammation# Pathogenesis- Germination of spores releases the exotoxin- Toxin affects nervous system and reaches CNS via the peripheral nerves- Acts on presynaptic terminals of inhibitor nerves- Reduces the release of inhibitory neurotransmitters (e.g., glycine)- Excess activity of motor neurons produces muscle spasm# Clinical features- Facial muscle spasm produces trismus- Typical facial appearance = 'risus sardonicus'- Back muscle spasm produces opisthotonous- Eventually exhaustion and respiratory failure leads to death- The diagnosis is essentially clinical- Differentiating between contamination and infection on wound swabs is difficult# Prevention:- Tetanus can be prevented by- Active immunisation with tetanus toxoid with booster every 5-10 years- Adequate wound toilet of contaminated wounds- Consider passive immunisation with hyperimmune immunoglobulin# Treatment (of suspected cases)- Passive immunisation with anti-tetanus immunoglobulin- Adequate wound debridement- Intravenous benzyl penicillin- Intensive care support- Despite the use of ITU mortality is about 50%