Bacterial toxins which affect the peripheral nervous system
produces the diphtheria toxin. This toxin consists of two joined subunits, A and B, which are split after endocytosis, allowing A to inhibit protein synthesis. Patients develop inflammation of the throat after inhalation of the bacteria.
Neurologic manifestations begin with palatal paralysis 1 to 2 weeks after symptom onset and then progress to ciliary body paralysis with loss of accommodation but preserved light reaction.
Six weeks after initial infection the patient may develop a descending paralysis and require mechanical respiratory support.
The illness will resolve if the patient does not succumb to cardiac and respiratory complications.
is introduced through a wound and produces tetanus toxin, a zinc-dependent protease that prevents release of gamma-aminobutyric acid by cleaving surface proteins on synaptic vesicles.
Local tetanus involves local stiffness and muscle spasms around a wound, resolving in weeks to months. Generalized tetanus begins locally and generalizes over a few days to involve full body spasms including the pharyngeal, laryngeal, and respiratory muscles.
is typically ingested through foods such as home-preserved items and produces the botulinum toxin. This toxin inhibits the release of acetylcholine from peripheral nerve endings at the neuromuscular junction.
Symptoms develop in 12 to 36 hours and typically begin as diplopia due to extraocular movement paralysis with progression to other bulbar muscles, then the neck, trunk, limbs, and respiratory muscles.
Del Brutto OH: Neurocysticercosis. Continuum (Minneapolis, Minn.) 18(6 Infectious Disease):1392-1416, 2012.