CLOSTRIDIUM TETANI

 

Properties

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment & Prevention

Gram-positive rods

 

Obligate anaerobes

 

Form spores

 

Long thin bacteria with large terminal spores.

Transmission:

- widespread in soil.

- found in faeces of farm animals & human gut.

- germination of spores is favored by necrotic tissue & poor blood supply in wound.

- neonatal tetanus: organism enters through contaminated or circumcision wound.

 

Produces neurotoxin tetanospasmin:

- site of action is lower motor neuron.

- binds to ganglioside receptors of CNS.

- toxin is a protease that cleave proteins associated with mediator release.

- blocks release of inhibitor mediators at spinal synapses.

- nerve cell fires continuously – muscle it supplies goes into a state of tetanic spasm.

Violent muscle spasms

 

Lockjaw due to rigid contraction of jaw muscles which prevent mouth from opening.

 

Facial spasms produce ‘sardonic grin’.

 

Respiratory failure ensures, high mortality rate.

No microbiologic or serologic diagnosis.

 

Organisms are rarely isolated from wound sites.

Treatment:

- remove dead & unhealthy tissue from wound.

- human tetanus immunoglobulin given to neutralize free toxin.

- benzylpenicillin given to kill any clostridia left.

- patients are sedated or ventilated till bound toxin is broken down.

- benzodiazepines given to prevent spasms.

 

Prevention:

- immunization with tetanus toxoid.

- clean & debride wound.

 

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