See food poisoning.
In a technique pioneered by Alan B. Scott, an ophthalmologist, and Edward Schantz, a biochemist, in the late 1970s, botulin toxin has been purified and used in the treatment of debilitating muscle spasms caused by the excessive firing of certain nerves. The treatment utilizes the same process that paralyzes the muscles in botulism poisoning. Injected in tiny amounts into the affected tissue, the botulin blocks the release of acetylcholine, a neurotransmitter that controls muscle contraction, and temporarily relieves the spasms. Botulin was approved by the Food and Drug Administration in 1989 for treatment of blepharospasm (uncontrolled rapid blinking) and strabismus (crossed eyes); it is under study for use in other spasmodic conditions. The toxin is also injected to provide short-term (three to four months) cosmetic treatment of facial wrinkles.
Poisoning by botulinum toxin, one of the most potent toxins known, produced by Clostridium botulinum bacteria. It usually results from improperly sterilized canned (mostly home-canned) foods. Heat-resistant spores of these anaerobic bacteria in fresh food may survive canning. The bacteria multiply and secrete toxin, which remains potent if the food is not well heated before it is eaten. Botulism can also result from wound infection. Botulinum toxin blocks nerve-impulse transmission. If botulism is recognized in time, administered antitoxins can neutralize it. The first symptoms of botulism are nausea and vomiting, which usually appear six hours or less after the contaminated food is eaten. Fatigue, blurry vision, and general weakness follow. Respiratory paralysis can cause death if not treated with emergency tracheotomy and respiratory aid. Most victims recover completely if they survive paralysis. The bacteria's intense toxicity makes it a potentially deadly biological warfare agent.
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There are three main kinds of botulism:
All forms of botulism can be lethal and are always considered medical emergencies. Foodborne botulism can be extremely dangerous as a public health risk because multiple persons can consume the poison from a single contaminated food source.
An average of 110 cases of botulism are reported each year in the United States. Of these, approximately, 72% are infant botulism, and 3% are wound botulism. Outbreaks of foodborne botulism involving two or more persons occur during most years and are usually caused by the consumption of home-canned foods. The number of cases of foodborne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of black tar heroin, especially in California. In July 2007, a widespread recall was initiated due to botulism contamination of food manufactured by Castleberry's Food Company. Shortly thereafter, in August 2007, the FDA issued a warning of botulism risk from canned French cut green beans manufactured by Lakeside Foods Inc, of Manitowoc, Wisconsin.
Normal symptoms usually include dry mouth, double and/or blurred vision, difficulty swallowing, muscle weakness, drooping eyelids, difficult breathing, slurred speech, vomiting, urinary incontinence and sometimes diarrhea. These symptoms may continue to cause paralytic ileus with severe constipation, and will lead to body paralysis. The respiratory muscles are affected as well, which may cause death due to respiratory failure. These are all symptoms of the muscle paralysis caused by the bacterial toxin.
In all cases illness is caused by the toxin made by C. botulinum, not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that are firing more often.
Honey, corn syrup, and other sweeteners are potentially dangerous for infants. This is partly because the digestive juices of an infant are less acidic than older children and adults, and may be less likely to destroy ingested spores. In addition, young infants do not yet have sufficient numbers of resident microbiota in their intestines to competitively exclude C. botulinum. Unopposed in the small intestine, the warm body temperature combined with an anaerobic environment creates a medium for botulinum spores to germinate, divide and produce toxin. Thus, C. botulinum is able to colonize the gut of an infant with relative ease, whereas older children and adults are not typically susceptible to ingested spores. C. botulinum spores are widely present in the environment, including honey. For this reason, it is advised that neither honey, nor any other sweetener, be given to children until after 12 months. Nevertheless, the majority of infants with botulism have no history of ingestion of honey, and the exact source of the offending spores is unclear about 85% of the time. Spores present in the soil are a leading candidate for most cases, and often a history of construction near the home of an affected infant may be obtained.
Besides supportive care, infant botulism can be treated with human botulism immune globulin (BabyBIG), when available. Supply is extremely limited, but is available through the California Department of Health Services. This dramatically decreases the length of illness for most infants. Paradoxically, antibiotics (especially aminoglycosides or clindamycin) may cause dramatic acceleration of paralysis as the affected bacteria release toxin. Visual stimulation should be performed during the time the infant is paralyzed as well, in order to promote the normal development of visual pathways in the brain during this critical developmental period.
Furthermore each case of food-borne botulism is a potential public health emergency in that it is necessary to identify the source of the outbreak and ensure that all persons who have been exposed to the toxin have been identified, and that no contaminated food remains.
There are two primary Botulinum Antitoxins available for treatment of wound and foodborne botulism. Trivalent (A,B,E) Botulinum Antitoxin is derived from equine sources utilizing whole antibodies (Fab & Fc portions). This antitoxin is available from the local health department via the CDC. The second antitoxin is heptavalent (A,B,C,D,E,F,G) Botulinum Antitoxin which is derived from "despeciated" equine IgG antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This is a less immunogenic antitoxin that is effective against all known strains of botulism where not contraindicated. This is available from the US Army. On 1 June, 2006 the US Department of Health and Human Services awarded a $363 million contract with Cangene Corporation for 200,000 doses of Heptavalent Botulinum Antitoxin over five years for delivery into the Strategic National Stockpile beginning in 2007.
Between 1910 and 1919 the death rate from botulism was 70% in the United States, dropping to 9% in the 1980s and 2% in the early 1990s, mainly because of the development of artificial respirators. Up to 60% of botulism cases can be fatal if left untreated.
The World Health Organization (WHO) reports that the current mortality rate is 5% (type B) to 10% (type A). Other sources report that, in the U.S., the overall mortality rate is about 7.5%, but the mortality rate among adults over 60 is 30%. The mortality rate for wound botulism is about 10%. The infant botulism mortality rate is about 1.3%.
One study showed that about 5% of children whose death was attributed to Sudden Infant Death Syndrome had actually died of botulism.
Death from botulism is common in waterfowl; an estimated 10 to 100 thousand birds are killed annually. In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock. Some affected birds may recover without treatment.
Botulism seems to be relatively uncommon in most domestic mammals; however, in some parts of the world, epidemics with up to 65% are seen in cattle. The prognosis is poor in large animals that are recumbent. Most dogs with botulism recover within 2 weeks.
Wound botulism can be prevented by promptly seeking medical care for infected wounds, and by avoiding punctures by unsterile things such as needles used for street drug injections. It is currently being researched at USAMRIID under BSL-4.
In cattle, the symptoms may include drooling, restlessness, inco-ordination, urine retention, dysphagia, and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and inco-ordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralysed and death may occur.
The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs.
Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis.
In poultry and wild birds, flaccid paralysis is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhoea with excess urates.