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| Botulism |  |
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.
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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.
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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.
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