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. |