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 poisoning.
Clostridium botulinum is actually quite common and endemic to many regions of the world. They are often found in soil, riverbeds, lake sediment, in coastal waters, and even within animals, fish and shellfish. The organism was first isolated from a ham identified as the source of a botulism poisoning outbreak in 1895. Further study of the organism found it was an anaerobic spore producing rod bacterium.
The spores produced by Clostridium botulinum are heat resistant and able to survive and remain viable in very adverse conditions, including boiling at sea level. As such, safe canning procedures often require pressurization in addition to boiling which can kill off the spores and prevent production of botulinum in food products.
Since Clostridium botulinum is an anerobe, it is only able to grow, produce spores and produce toxin in oxygen free environments, hence why canned goods are often an ideal environment for the organism to grow. High levels of oxygen, high amounts of sugar, high acidity, extremely low moisture and low temperature below 3 degree Celsius inhibit the growth and production of Clostridium botulinum spores and toxins.
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 of Botulism Poisoning
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 poisoning.
The autonomic effects of botulism poisoning 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.
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./li>
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.
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 poisoning.
The autonomic effects of botulism poisoning 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.
