Disease Description

Botulinum toxins are a group of seven related neurotoxins (Types A-G) produced by the bacterium, Clostridium botulinum. Most cases of human botulism is caused by toxins types A, B, D or F. These toxins are the most potent neurotoxin known. The toxin can be formed in canned foods and subsequently ingested. The clinical syndrome produced by these toxins is known as botulism.

• Food-borne botulism
  Occurs when a person ingests pre-formed toxin.
   
• Infant botulism
  Occurs when susceptible infants consumed C. botulinum spores.
   
• Wound botulism
  Caused by the growth of C.botulinum bacteria in a wound

In addition, botulinum toxins can also be inhaled if intentionally released in the form of aerosol.

Incubation Period

• lnhalational botulism: time to onset of paralytic symptoms after inhalation may actually be longer than for foodborne cases. Symptoms may appear 12 hr - 36 hours or longer after exposure.
   
• Food-borne botulism: symptoms appear 2 hr - 10 days (average 12 - 72 hours) after exposure.

Clinical Features

• Cranial nerve palsies are prominent in the early stages of disease. Symptoms include blurred vision due to mydriasis, diplopia, ptosis, and photophobia and dysarthria, dysphonia, and dysphagia. Flaccid skeletal muscle paralysis follows, in a symmetrical, descending, and progressive manner. Collapse of the upper airway may occur due to weakness of the oropharyngeal musculature. As the descending motor weakness involves the diaphragm and accessory muscles of respiration, respiratory failure may occur abruptly. Progression from onset of symptoms to respiratory failure has occurred in as little as 24 hours in cases of severe food-borne botulism.
   
• The autonomic effects of botulism are manifested by typical anticholinergic signs and symptoms such as dry mouth, ileus, constipation, and urinary retention. Nausea and vomiting may occur as non-specific sequelae of an ileus. Dilated pupils (mydriasis) are seen in approximately 50 percent of cases. Sensory symptoms usually do not occur.
   

Differential Diagnosis

Guillain-Barre, myasthenia gravis, stroke, organophosphate poisoning, magnesium intoxication, atropine poisoning.


Laboratory investigations

• Blood and faeces for culture.
   
• Serum can also be sent to identify toxins.
   

Management

• Supportive care, including prompt respiratory support. Intensive and prolonged nursing care may be required for recovery. This may takes up to three months for the initial signs of improvement and up to a year for complete resolution of symptoms.
   
• Antitoxin, early administration is critical to neutralise circulating toxin in patients with symptoms that continue to progress. Antitoxin is less likely to be of benefit if given >72 hours after the onset of symptoms.
   

Prophylaxis

• A pentavalent toxoid of C.botulinum toxin types A,B,C,D and E is available as an investigational agent for pre-exposure prophylaxis. The currently recommended primary series of 0,2 and 12 weeks followed by booster at 1 year.
   
• Human data are not available to support the recommendation of post-exposure prophylaxis with heptavalent antitoxin.
   

Isolation precautions

• Secondary aerosols from affected patients pose no risk of botulism transmission. Toxin is not absorbed through the skin. There is no risk of person-to person transmission.
   
• Standard precautions for Healthcare workers
   
• Decontamination of surfaces contaminated by the toxin can be achieved using soap and water or 0.5% hypochlorite solution.
   
• If contamination of foodstuffs suspected, boiling foods for 10 minutes will destroy toxins.
   
• Quarantine is not necessary.

Case Fatality

High mortality if no respiratory support.