Acute neurological process with neuroparalytic due to a neurotoxin produced by Clostridium botulinum.
Neurotoxin binds irreversibly to presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions.
C botulinum is an anaerobic gram positive rod that survives in the soil and marine sediment by spore formation.
Under anaerobic conditions C botulinum germinates and releases an exotoxin.
The botulinum organism stains gram positively early , but may be gram negative after 18 hours of incubation, making diagnosis more complicated.
The binding of the neurotoxin blocks acetylcholine release with weakness, paralysis and possible respiratory arrest.
The toxin mediated infection causes blockage of the transmission of acetylcholine across cholinergic synapses of the peripheral nervous system resulting in descending, flaccid, symmetric pattern of paralysis, with prominent bulbar palsy.
Associated with loss of ocular accommodation, diplopia, blurred vision, dysphonia, dysarthria, and facial weakness.
The sensorium is unaffected.
3 presentations of the disease are infant type, foodborne and wound type.
Infant type related to ingestion of C botulinum spores that germinate in the intestine.
Infant type usually results in full recovery with supportive care and a mortality rate of less than 1%.
In the infant type the spores come from bee honey or the environment.
Foodborne botulism related mainly to improperly canned foods or contaminated home prepared foods.
Wounds contaminated with toxin producing C botulinum associated with wound botulism.
Foodborne disease and wound disease occur primarily in adults.
There are eight antigen specific C botulinum toxins: A, B, C (alpha), C (beta), D, E, F and G.
Types A, B,E, cause disease, and F rarely does so.
Type A and B toxins are the most potent.
Toxin A most commonly involved with foodborne outbreaks, followed by B and E.
In 15% of cases no toxin is identified.
Type G botulinum toxin associated with sudden deafness.