Why did this condition - all on its own - merit an entire chapter of Oh's Manual? One might conjecture that tetanus, though essentially unknown in the developed west, is still prevalent in the rest of the world and therefore worth mentioning in any textbook which lays claim to global appeal. As an introduction to tetanus, Oh's is comprehensive. But, for those of us who have little time, the LITFL review of tetanus is an excellent condensed resource. And for those of us with infinite time, the references below are comprehensive and most importantly interesting. Question 12 from the second paper of 2013 and Question 6 from the second paper of 2017 explored this issue extensively, and it may come up again even though its relevance to metropolitant Australian intensive care may be minimal
In short: after spending some of its life cycle in dirt or faeces, C.tetani spores find their way into an open wound, and take root there. It used to be rusty nails animal bites and battlefield injuries, but these days body modification piercing (particularly of mucous linings) is the prevalent cause. The spores reproduce. Approximately 10-15 days after the first infection, they generate the "vegetative form" which is the true bacillus; this form secretes tetanospasmin, the tetanus toxin responsible for the horrific signs and symptoms.
The first few signs and symptoms are:
The latter is due to masseter spasm.
Later, more muscle groups become involved, in a roughly descending manner.
These signs and symptoms all arise from the effect of tetanus toxin on synaptobrevin, a protein which faciliates the binding of neurotransmitter vesicles to the presynaptic membrane. The consequence is a cessation of neurotransmission - particularly of GABA.
The decrease in inhibition is equivalent to excitation. This mechanism is well described in a review article form the BMJ. The decrease in GABA activity accounts for the increase in motor tone, and for the dyregulation of postural and autonomic reflexes. The tetanus toxin also acts as an inhibitor of presynaptic acetylcholine release at the neuromuscular junction, which under normal circumstances might produce flaccid paralysis (like botulinum toxin) - but the central disinhibition overrules any peripheral neuromuscular junction dysfunction, and rigidity still ensues.
There are several syndroms which can also account for whole-body rigidity, opisthotonos and trismus. These were asked about in Question 6 from the second paper of 2017.
Rodrigo, Chaturaka, Deepika Fernando, and Senaka Rajapakse. "Pharmacological management of tetanus; an evidence based review." Crit Care18 (2014): 217.
Cook, T. M., R. T. Protheroe, and J. M. Handel. "Tetanus: a review of the literature." British Journal of Anaesthesia 87.3 (2001): 477-487.
Wesley, A. G., et al. "Labetalol in tetanus." Anaesthesia 38.3 (1983): 243-249.
Attygalle, D., and N. Rodrigo. "Magnesium as first line therapy in the management of tetanus: a prospective study of 40 patients*." Anaesthesia 57.8 (2002): 778-817.
Henderson, Sean O., et al. "The presentation of tetanus in an emergency department." The Journal of emergency medicine 16.5 (1998): 705-708.
Apte, Nitin M., and Dilip R. Karnad. "The spatula test: A simple bedside test to diagnose tetanus." The American journal of tropical medicine and hygiene 53.4 (1995): 386-387.