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Botulism

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Botulism

Uncommon disease caused by preformed exotoxins produced by Clostridium botulinum

Aetiology

- disease caused mostly be type A, B and E exotoxin
- spores are moderately resistant to heat (ie they withstand boiling for several hours
- vast majority food-bourne. Outbreaks largely due to home-preserved vegetables (type A), meat (B) or fish (E)
- other high risk foods include low acid fruit and condiments
- wound botulism (rare) due to contamination of wound with soil containing type A or B organisms
- chronic IV drug abusers at risk

Pathophysiology

- exotoxin absorbed in gut and carried to cholinergic nerves at NMJ, post ganglionic nerve endings and autonomic ganglia to which it binds irreversibly
- toxin enters nerve endings and interferes with ACh release

Clinical features

- usually 3 day incubation after ingestion of toxin. Range 12h-16 days
- GI symptoms (food-bourne botulism only): nausea, vomiting, abdo pain, diarrhoea or constipation
- ocular symptoms: blurred vision, mydriasis, diplopia, ptosis
- dry mouth
- dysphagia
- impaired gag, facial and tongue weakness
- generalised weakness. Progresses in a symmetrical descending fashion. Reflexes normal/decreased
- severe cases: respiratory insufficiency and flaccid weakness of limbs

Differential diagnosis

- other causes of food poisoning
- myasthenia
- GBS

Investigations

- detection of toxin in patient or food
- CSF normal apart from mild elevation of CSF protein in a few cases
- edrophonium test -ve although transient less impressive responses may be seen in botulism patients
- ECG: may be minor conduction disturbances and non-specific T wave and ST changes
- nerve conduction normal
- EMG: presynaptic block in affected muscles in only 1/3
- detection of Cl botulinum in stool considered confirmatory

Management

- intubation and ventilation: if bulbar palsy significant or if VT < 10-15 ml/kg in association with hypercarbia and hypoxia. Risk of respiratory failure greatest in first 2 days of hospitalization
- correct fluid and electrolyte imbalance
- in absence of profound ileus, removal of unabsorbed toxin can be attempted with water, saline or cathartic enemas. Avoid Mg containing preparations
- antitoxin. If symptoms are severe and toxin type is known given monovalent antitoxin. Otherwise equine trivalent antitoxin. Dose can be repeated 4 hrly if patient continues to deteriorate Efficacy of antitoxin in humans not proven in controlled studies except for type E toxin illness. Hypersensitivity reactions occur in 9% and therefore antitoxin should not be used in mild cases. History of atopic illness or previous administration of equine serum are relative contraindications. Full resuscitation facilities should be available
- guanidine enhances release of ACH from nerve terminals and appears to be particularly effective in decreasing ocular weakness. May be more appropriate in mild cases than antitoxin
- antibiotics only for specific infectious complications. Penicillin generally given. Efficacy unproven
- wound debridement

Prognosis

- most patients improve within a week or so
- small minority require ventilatory support
- factors associated with poorer prognosis: short incubation period, early involvement of cranial nerves and respiratory muscles, increased age and ? Asian race
- ICU survival rate should be high and outlook for complete recovery good
- general weakness, mild cranial palsies, constipation

Infant botulism

- 1 week to 9 months. 95% < 6 months
- type A and B
- honey ingestion considered a risk factor
- spores germinate and produce toxins in infant's gut
- may present with features ranging in severity from constipation to sudden death
- neuro signs usually appear after 1-3 weeks (weak cry, impaired sucking, drooling, "floppy" head)
- differential includes: sepsis, infectious mononucleosis, virus infections, organisms
- toxin rarely detected in serum
- symptomatic treatment
- mortality about 2%

Further reading

Skrowronski GA. Neuromuscular disorders. In Oh TE (ed). Intensive Care Manual, 4th ed., 1997. Butterworth Heinemann, Oxford. pp 434-9


© Charles Gomersall November 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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