organisms, yeasts or moulds, growing in the product and increasing
the pH.
The maximum pH for growth is 8.5–8.9 and the toxin is unstable at
alkaline pH values. This is generally an unimportant feature of the
organism’s physiology since nearly all foods are slightly acidic. It may be
significant however in some North American fermented fish products
occasionally associated with botulism where the usual increase in pH on
fermentation would be a protective factor.
7.5.3 Pathogenesis and Clinical Features
Three types of botulism are recognised: foodborne botulism, infant or
infectious botulism and wound botulism. Only in the first type is food
invariably involved.
Foodborne botulism is an example of bacterial food poisoning in its
strictest sense: it results from the ingestion of an exotoxin produced by
Clostridium botulinumgrowing in the food. The botulinum toxins are
neurotoxins; unlike enterotoxins, which act locally in the gut, they affect
primarily the cholinergic nerves of the peripheral nervous system.
Experiments in animals have shown that toxin ingested with food and
surviving inactivation is absorbed in the upper part of the small intestine
and reaches the bloodstreamviathe lymphatics. It binds to the nerve
ending at the nerve–muscle junction, blocking release of the acetylcholine
responsible for transmission of stimuli, thus producing a flaccid paralysis.
Initial symptoms of botulism occur anything from 8 h to 8 days, most
commonly 12–48 h, after consumption of the toxin-containing food.
Symptoms include vomiting, constipation, urine retention, double vision,
difficulty in swallowing (dysphagia), dry mouth and difficulty in speaking
(dysphonia). The patient remains conscious until, in fatal cases, shortly
before the end when the progressive weakness results in respiratory or
heart failure. This usually occurs 1–7 days after the onset of symptoms.
Surviving patients may take as long as 8 months to recover fully.
The clinician can do little to mitigate the effect of toxin already
adsorbed at the neuromuscular junction, although neuromuscular block-
ade antagonists such as 4-aminopyridine have produced transient
improvements. Survival is therefore critically dependent on early diag-
nosis and treatment, principally by alkaline stomach washing to remove
any remaining toxic food, intravenous administration of specific or
polyvalent anti-toxins to neutralize circulating toxin, and mechanical
respiratory support where necessary.
The mortality rate is usually high (20–50%), but will depend on a
variety of factors such as the type of toxin (type A usually produces a
higher mortality than B or E), the amount ingested, the type of food and
the speed of treatment.
202 Bacterial Agents of Foodborne Illness