Tetanus (lockjaw) is an acute clostridial disease, its clinical manifestations do not result directly from the invasive infection, but are rather caused by a strong neurotoxin.
Toxin. Tetanospasmin (an AB toxin, p. 16) consists of two polypeptide chains linked by a disulfide bridge. The heavy chain binds specifically to neuron receptors. The light chain is a zinc-metalloprotease that is responsible for pro-teolysis of components of the neuroexocytosis apparatus in the synapses of the anterior horns of the spinal cord. This stops transmission of inhibitory efferent impulses from the cerebellum to the motor end plates.
Pathogenesis and clinical picture. These ubiquitous pathogens invade tissues following injuries (Fig. 4.8a). Given anaerobic conditions, they proliferate and produce the toxin (see above), which reaches the anterior horns of the spinal cord or brain stem via retrograde axonal transport. The clinical picture resulting from the effects of the toxin is characterized by increased muscle tone and spasms induced by visual or acoustic stimuli. The cramps often begin in the facial musculature (risus sardonicus, Fig. 4.8b), then spread to neck and back muscles (opisthotonus). The patient remains lucid.
Diagnosis. The preferred method is toxin detection in wound material in an animal test (mouse) based either on neutralization or detection of the toxin gene with PCR. The pathogen is difficult to culture.
Therapy. Antitoxic therapy with immune sera is applied following a meticulous wound cleaning. The patient's musculature must also be relaxed with curare or similar agents.
Fig.4.8 a Open lower-leg fracture following a traffic accident; the portal of entry of C. tetani.
b Risus sardonicus: fully manifest case of tetanus in a patient with lower-leg fracture. Patient was not vaccinated.
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