Clostridium Botulinum
Clostridium botulinum has eight different serotypes of neurotoxins (labelled A to H) although cases caused by type G have not yet been reported in humans. Type C causes disease in birds. Type D causes bovine botulism disease. Type E is most often found in marine environments. Type A is the most toxic substance known to man. An amount equivalent of a few grains of sugar would be enough to kill at least twenty-five people. On a weight by weight basis, this makes it 15,000 times more potent than VX nerve gas and 100,000 times more powerful than the nerve gas Sarin, the agent used in the terrorist attack in the subway system of Tokyo in 1995.
C. botulinum is able to grow in such various environments as animal feeds, carcasses of dead animals or invertebrates, and sediments in lakes or ponds. Outbreaks of the disease occur when these contaminated materials are eaten by other animals or birds. Such wildlife outbreaks, where the deaths of hundreds of thousands of wild ducks, for example, are commonly caused by the botulinum toxin types C and D.
Botulism is the Latin word for sausage (botulus) named about 200 years ago after an outbreak in Europe was linked (no pun intended) to bad sausage and fish. The optimum temperature for toxin reproduction is 30°C (86°F), but some toxins can be produced at temperatures as low as 3°C (37.4°F), usually in fish. Toxins can be destroyed by heating foods to 80°C (176°F) for 1 minute or by simmering prepared foods for twenty minutes. Salt, as well as nitrates, also destroy the toxins -- which is the reason nitrates are put into hot dogs. C. botulinum is considered a poisoning rather than an infectious disease because transmission from person to person does not occur. Epidemic-type outbreaks occur as a result of contaminated food being eaten by a number of people or animals. Usually, when humans become infected, it is as a result of eating improperly home-preserved foods. The microbes release a gas characterized by a bulge in tins, but its presence is more difficult to detect in glass canning jars. Immunity does not result from the illness because the amount needed to trigger a response from the immune system is much more than would cause death.
The toxin, generally from serotypes A,B, or E, is directly absorbed primarily from the small intestine, passes into the blood, and is carried to the peripheral nerves, where it specifically reacts at the muscle-nerve junction. Symptoms may appear as soon as twelve to thirty-six hours after ingesting contaminated food, it or may take as long as eight days to appear. The first symptoms of botulism poisoning are often weakness and dizziness. Double vision (diplopia), difficulty in speaking (diphonia) and swallowing (dysphagia), and dilated pupils usually occur as well. There may be some abdominal discomfort but rarely any fever. The toxin produces complete paralysis of the nerve impulse by preventing the release of acetylcholine. Muscle weakness then develops, and, as the disease progresses, paralysis becomes more apparent and widespread. When the paralysis reaches the respiratory system, death results. Patients usually remain fully conscious until just before death, compounding the agony. Death rate varies between 20% and 70%, depending on the amount and serotype of the toxin consumed, as well as the length of time between ingestion and antitoxin therapy. Therapeutic treatment involves an antitoxin to types A, B, and E, since it is usually one of those three responsible for illness. The antitoxin will not reverse the effects of the toxin already affecting the nerves, but it will neutralize any circulating toxin.
In 1976, it was discovered that C. botulinu could grow in the intestines of infants, producing enough toxin to cause serious illness. Unpasteurized honey is often the culprit, but other infant foods have also been implicated. Not all infants are susceptible, however, and it is not known exactly what the predisposing factors may be. Signs of the disease begin with constipation, followed by weakness, and then paralysis of the head and neck muscles. Paralysis spreads to the arms and legs; and when it reaches the respiratory system, death results. In slow progessing cases, medical intervention can be applied in time, but, in rapidly developing cases, death often results before any significant symptoms are apparent. Some of these deaths come under the heading of SIDS since very few physicians have ever seen a botulism case.
An interesting use of the botulism toxin is one practised by dermatologists to smooth out facial wrinkles. The toxin is injected into the muscles, causing paralysis so that wrinkles do not form. These dermatologists like to call their patients in on the same day to have the treatment done since the toxin rapidly loses potency after the bottle is opened. The treatment is only guaranteed for three to six months, and then has to be done again -- a very risky price to pay for the illusion of a "fountain of youth."
A Canadian study has gone even further. Boxtox is now being studied as an inovative, but temporary, solution involving the numbing or deadening of glands and muscles. In an article published in the medical journal Pediatric Neurology, doctors in Halifax stated that the toxin could help reduce the drooling in children suffering from cerebral palsy. "When children drool profusely, it can detract from their physical appearance and often inhibits others from initiating social contact or showing affection to the child," said researchers at Izaak Walton Killiam Health Center. They also gave an additional impressive list of conditions that this "miracle cure" could alleviate -- migraines, uncontrollable blinking, crossed eyes, excessive sweating, tics and spasms, and stroke recovery. This study focused on nine children aged four to seventeen. All had some form of mental retardation, and all showed a decrease in drooling within the first month. Five of the nine showed a sustained improvement over a sixteen-week period, with the parents of these five eagerly awaiting reinjections of the toxin on their children. (From an article in the National Post, Aug. 10, 2002)
