Botulinum toxins block nerve functions and can lead to respiratory and muscular paralysis.
Human botulism may refer to foodborne botulism, infant botulism, wound botulism, and inhalation botulism or other types of intoxication.
(Choice A) Botulinum toxin irreversibly blocks acetylcholine release from presynaptic membranes of neuromuscular junctions.
After exposure to the toxin, patients may develop cranial nerve abnormalities (including ptosis and facial weakness), symmetric descending weakness, and respiratory failure. However, autonomic abnormalities are common, and symptoms are rapidly progressive (hours rather than weeks) and do not worsen with repetition.
The action of acetylcholine at the postsynaptic membrane is terminated by acetylcholinesterase, not by acetylcholine reuptake. Organophosphates (eg, pesticides, sarin gas) irreversibly inactivate acetylcholinesterase, causing cholinergic toxicity (eg, increased glandular secretions, widespread smooth muscle activation). Muscle weakness, including respiratory failure, can occur due to depolarizing blockade at the neuromuscular junction; however, other symptoms (eg, diarrhea, urination, miosis, bradycardia, emesis, salivation) would be expected.
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