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Home › Topics › Infectious Diseases › Infections A-Z › Botulism (Deliberate Releases) ›Guidance ›  Clinical Features of Disease
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Clinical Features of Disease

Forms of disease

Clinicians should be aware of the possibility of cases of botulism.

Any previously healthy patient with the following classic triad should be immediately reported to the Consultant in Communicable Disease Control at the local Health Protection Unit.

  • symmetrical descending flaccid paralysis with prominent bulbar palsies including diplopia, dysarthria, dysphonia and dysphagia
  • afebrile
  • no change in sensory awareness

Gastrointestinal symptoms occur in food-borne and intestinal colonisation botulism. Nausea, vomiting and diarrhoea followed by constipation arise in food-borne botulism, however ingestion of large amounts of toxin may lead directly to neurological symptoms, and the diagnosis should be considered in the absence of gastrointestinal symptoms. In intestinal botulism in infants, several days of profound constipation may precede neurological symptoms.

Neurological symptoms are the same irrespective of the route of entry of toxin, but may develop more quickly in the event of inhalation, depending on the dose. Symptoms are of a descending, symmetrical flaccid paralysis:

  • Cranial nerve palsies produce diplopia, ptosis, facial weakness, dysphagia and dysarthria.
  • This is followed by weakness in the neck and arms, after which respiratory muscles and muscles of the lower body are affected.
  • In some cases, weakness in the neck and arms may be followed by respiratory paralysis or respiratory arrest and then by ptosis.
  • In some cases, marked respiratory compromise or respiratory arrest may occur before typical oculobulbar weakness and weakness in limbs.
  • There is no fever and no loss of sensory awareness.

Autonomic signs may be present, with dry mouth, fixed or dilated pupils, and cardiovascular, gastrointestinal and urinary autonomic dysfunction. Respiratory paralysis may be fatal.

Onset of gastrointestinal and neurological symptoms may be between 6 hours and 8 days. If onset is very rapid, there may be no symptoms before sudden respiratory paralysis occurs.

Mortality

Without treatment mortality can reach 100%, but this can be considerably reduced with supportive treatment and the use of antitoxin.

The lethal dose of C. botulinum toxin for an adult can be less than 1 microgram, depending on toxin type and route of administration. Exposure of rhesus monkeys to aerosols of botulinum toxin has shown that type F is about 60 times more toxic than typeBandtheorderoftoxicityisF>C>A>D>B.

Antimicrobial susceptibilities

In cases of botulism which result from ingestion (in food or water) or inhalation of toxin, antibiotic therapy is not appropriate.

In cases of wound infection, C. botulinum is susceptible to benzyl penicillin and metronidazole, which should be used together with surgical debridement.

Intestinal colonisation botulism results from colonisation of the gut by vegetative cells. Risk factors are not completely understood, but changes in gut flora around the time of weaning may permit colonisation. Another factor may be decreased gut motility which results in increased anaerobicity in the gut. Antibiotic therapy is not appropriate, because there is a risk of further reducing the normal gut flora and therefore increasing susceptibility to colonisation, and because lysis of vegetative cells killed by antibiotics may result in release of toxin.


Last reviewed: 1 April 2009