Botulinum neurotoxin is the most potent natural toxin of which we are aware.3
One mouse-unit of botulism neurotoxin killed 50% of 18- to 20-g mice in a test; for humans, thirty to forty mouse-units is deadly,3 and it only takes a few nanograms to make someone ill.25 Odorless and tasteless, the toxin can withstand both stomach acids and the digestive enzymes in the gastrointestinal tracts.6
This fearsome toxin is produced by spores of the rod-shaped, gram-positive bacterium Clostridium botulinum,25 a relative of tetanus,11 which are commonly found in the soil. When they infiltrate improperly-prepared home-canned vegetables, sausages, and meat and seafood products, they begin to reproduce, which releases the toxin. Factors that encourage this reproduction include an anaerobic environment, a pH of 4.6 or higher, warm temperatures, a high moisture content, and a lack of competing bacteria.25 Low-acid vegetables like okra and asparagus are prime hosts for botulinum toxin.20 However, the sugar content of jams and jellies precludes C. botulinum from growing in them, so they can be home-canned without risk.7
Botulism's history is very recent, as it is easily mistaken for other ailments and was rarely diagnosed properly. Certainly there was an outbreak in 1793 in the town of Wildebad, Germany. People became sick after eating contaminated sausages,21 and it is from this that botulism eventually got its name: the root word is "botulus," Latin for "sausage".8 In its early days, though, botulism was known by "Kerner's disease" because reports of the deaths by spoiled sausage were compiled by health official Justinius Kerner.1
It was not until 1895 that the causative organism was discovered. An epidemic in Ellezelles, Belgium, involving preserved ham, prompted the investigation which uncovered C. botulinum.8 26 The man who isolated the bacterium was Emile Pierre Marie van Ermengem, a bacteriology professor at the University of Ghent.21 Although not recognized in the United States until 1899,1 the flurry of interest in this ailment has hardly diminished since the days of Ermengem's discovery. Botulinum toxin has even been implicated as the cause of Gulf War Syndrome, for it composed part of the inoculations given to soldiers in the war.4
The incubation period for botulism averages between twelve to thirty-six hours19, although it may be as few as four hours or as many as eight days.25
Botulism is divided into four categories: foodborne botulism (which also affects nonhuman animals), infant botulism, wound botulism, and an unclassified variety which seems to colonize the intestines of adults in a similar fashion to infant botulism. As for the organism itself, there are seven types of C. botulinum recognized. As a handy reference:
|TYPE||WHO DISCOVERED IT?||YEAR|
|C||Bengston and Seldon||1922|
|F||Moller and Scheibel||1960|
|G||Giménez and Ciccarelli||1970|
Types A, B, E, and sometimes F affect humans,8 and there are several differences between the four types: for example, type A is more severe than type E, but E has a shorter incubation period than A.30 Type C affects birds and domestic animals. D is rare but usually affects cattle. (There have been two cases of C and D - one case each - affecting humans.) G has been found in Argentinian soil. There are also two other species of Clostridium - Clostridium baratii and Clostridium butyricum - that cause botulism-like symptoms in humans,8 although C. baratii has only been implicated in three cases, two of them infants.15 One of the largest outbreaks of type E botulism occurred in 1991 Egypt, a country which had had no history of botulism. After eating a traditional salted fish dish, 91 people contracted botulism and 18 died.29
In the United States, the foods most commonly involved in foodborne botulism are asparagus, beets, corn, fish, fish eggs, green or string beans, mushrooms, seal flippers and seal oil, peppers, tomatoes and tomato juice.21 62% of cases in the USA are caused by type A botulism.23 In one unusual case involving dairy products, eight people contracted botulism after consuming contaminated cheese sauce. Although rare, cases of botulism involving commercially prepared food are given high priority because they have the potential to affect a large number of people. In the Annals of Internal Medicine, John Townes advises that "Detecting and reporting even mild cases of botulism can stop outbreaks and prevent severe illness and deaths."24 This does seem to have worked, as the fatality rate for people with botulism dropped from 71% in the 1900s to 16% in the 1970s.8 There are, of course, other reasons for this, which will be discussed further on.
The milder symptoms of botulism include muscle weakness, difficulty speaking and swallowing, double and blurred vision, and progressive weakness ending in paralysis. Like tetanus toxin, C. botulinum toxin "causes paralysis by binding to receptors on nerve endings, entering the nerve, and interfering with the release of neurotransmitter." Further symptoms which may develop include gastrointestinal upset, vomiting, constipation (or, sometimes, diarrhoea), dry mouth, orthostatic hypotension, and urinary retention. Mental functions are not impaired, however, and, without problematic secondary complications, patients remain alert. Similar symptoms are caused by Guillain-Barré Syndrome, myasthenia gravis, tick paralysis, drug reactions, stroke, or nervous system infections.8 For further examples, see these case studies.
Botulism intoxication (rather than "infection," which it is not) can be verified by testing a patient's stool or serum for the toxin.8 A reliable test is the mouse neutralization test, in which samples of the suspect food are injected into mice to see if they become intoxicated. Following this 48-hour test, samples of the food are cultured and monitored for C. botulinum, which takes from five to seven days.25
Botulism patients are treated with a trivalent botulism antitoxin, which stops botulism toxin from binding to nerve receptors. The antitoxin must be administered quickly because it cannot destroy the toxin once it has become attached or reverse existing symptoms, although it can stop further symptoms from developing. The Centers for Disease Control in Atlanta recommends 10,000 IU each of type A, B and E antitoxin.8 There has been some concern over administering the antitoxin to pregnant women - would it cause problems in her unborn baby? Recent incidents have indicated the opposite: women late into their pregnancies were given botulinum antitoxin and when their children were born, the infants had not sustained any damage. It is still unclear, however, if the antitoxin would be equally safe for women in the earlier halves of their pregnancies. 16 17
A full description of medical treatment for botulism was given by Carol O. Tacket and Michael A. Rogawski in source 20.
A vaccine for botulism does exist, but because of the rarity of the ailment, it is not practical to implement on a large scale.8 Besides, the amount of toxin required to make someone immune to botulism would be fatal.23 All that is really needed is a good dose of prevention. An article in the Journal of the American Medical Association states, "Cooked foods should not be held at temperatures 40 degrees F to 140 degrees F for greater than four hours. Boiling food for 10 minutes before eating destroys any toxin present."7 The spores, however, cannot be destroyed unless heated to very high temperatures, which can only be done using a device such as a pressure cooker.22 This is the reason why canning must be done so carefully.
Despite the terrifying dangers of botulism that can put people off canned food for the rest of their lives, even this dark cloud has its silver lining. In December 1989, the United States Federal Drug Administration approved type A toxin for use in treating strabismus, blepharospasm and hemifacial spasm in patients over twelve years old. The toxin affects only the unrestrainable muscle, providing relief to patients.3
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