botulism

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Definition

Botulism is caused by botulinum toxin, a natural poison produced by certain bacteria in the Clostridium genus. Exposure to the botulinum toxin occurs mostly from eating contaminated food, or in infants, from certain clostridia growing in the intestine. Botulinum toxin blocks motor nerves' ability to release acetylcholine, the neurotransmitter that relays nerve signals to muscles, and flaccid paralysis occurs. As botulism progresses, the muscles that control the airway and breathing fail.

Description

Botulism occurs rarely, but it incites concern because of its high fatality rate. Clinical descriptions of botulism possibly reach as far back in history as ancient Rome and Greece. However, the relationship between contaminated food and botulism wasn't defined until the late 1700s. In 1793 the German physician, Justinius Kerner, deduced that a substance in spoiled sausages, which he called wurstgift (German for sausage poison), caused botulism. The toxin's origin and identity remained elusive until Emile von Ermengem, a Belgian professor, isolated Clostridium botulinum in 1895 and identified it as the poison source.

Three types of botulism have been identified: food-borne, wound, and infant botulism. The main difference between types hinges on the route of exposure to the toxin. In the United States, there are approximately 110 cases of botulism reported annually. Food-borne botulism accounts for 25% of all botulism cases and can be traced to eating contaminated home-preserved food. Infant botulism accounts for 72% of all cases, but the recovery rate is good (about 98%) with proper treatment.

Though domestic food poisoning is a problem world-wide, there has been a growing concern regarding the use of botulism toxin in biological warfare and terrorist acts. The Iraqi government admitted in 1995 that it had loaded 11,200 liters of botulinum toxin into SCUD missiles during the Gulf War. Luckily, these special missiles were never used. As of 1999, there were 17 countries known to be developing biological weapons, including the culture of botulism toxins.

— Janie Franz

A severe, sometimes fatal food poisoning caused by ingestion of food containing botulin and characterized by nausea, vomiting, disturbed vision, muscular weakness, and fatigue.

[German Botulismus, from Latin botulus, sausage.]

Definition

Botulism is a neuroparalytic disease caused by the potent toxin of the Clostridium botulinum bacterium. There are three main types of botulism: foodborne botulism, infant botulism, and wound botulism.

Description

Botulism was first identified in Wildbad, Germany, in 1793, when six people died after consuming a locally produced blood sausage. In 1829, Jutinius Kerner, a health official, described 230 cases of sausage poisoning. Thereafter, the illness became known as "botulism," which is derived from the Latin "botulus," meaning sausage. In 1897, E. Van Ermengem identified the bacterium and its toxin while investigating an outbreak of the disease among musicians in Elezells, Belgium.

C. botulinum is a spore-forming, anaerobic, grampositive bacilli found globally in soil and honey. The toxin has recently gain notoriety. It is a potential bioterrorism agent, and it is used as a beauty aid to eliminate frown lines.

Clinically, food-borne botulism is dominated by neurological symptoms, including dry mouth, blurred vision and diplopia, caused by the blockade of neuromuscular junctions.

In wound botulism the neurologic findings are similar to the food-borne illness, but the gastrointestinal symptoms are absent. Infants suffering from the intestinal colonization of spores of C. botulinum suffer first from constipation, and later develop neurological paralysis, which can lead to respiratory distress.

There are seven distinct neurotoxic serotypes, all of which are closely related to the tetanus toxin. Types A and B are most commonly implicated, but types E and, more rarely, F have been associated with human disease.

Demographics

Botulism is rare, but its incidence does vary by geographic region. The food-borne version remains highest among people who can their own foods. In 1995, only 24 cases of food-borne botulism were reported to the Centers for Disease Control and Prevention.

About 90% of global cases of infant botulism are diagnosed in the US, where the annual incidence is about 2 per 100,000 live births. It is the most common form of human botulism in the United States, with over 1,400 cases diagnosed between 1976 and 1996.

Between 1943 and 1985, 33 cases of wound botulism were diagnosed in the United States, mainly associated with deep and avascular wounds. However, between 1986 and 1996, 78 cases of wound botulism were diagnosed, many the result of illicit drug use, occurring at injection sites or at nasal or sinus sites associated with chronic cocaine snorting.

Causes and symptoms

Botulism is caused by the protein toxin released by the microorganism C. botulinum. After the toxin is absorbed into the bloodstream, it irreversibly binds to the acetylcholine receptors on the motor nerve terminals at neuromuscular junctions. After the toxin is internalized, it cleaves the apparatus in the neuron that is responsible for acetylcholine release, making the neuron unresponsive to action potentials. The blockade is irreversible and may last for months, until new nerve buds grow.

FOOD-BORNE BOTULISM The symptoms can range from mild to life threatening, depending on the toxin dose. Generally, symptoms appear within 36 hours of consuming food containing the toxin. Paralysis is symmetric and descending. The first symptoms to appear include dysphagia, dysarthria, and diplopia, a reflection of cranial nerve involvement. Neck and limb weakness, nausea, vomiting, and dizziness follow. Respiratory muscle paralysis can lead to ventilatory failure and death unless support is provided.

WOUND BOTULISM The in vivo production of toxin by C. botulinum spores, leads to the neurologic symptoms seen in food-borne botulism. Gastrointestinal symptoms are absent.

INFANT BOTULISM Peak incidence occurs between 2 and 3 months of age. C. botulinum spores colonize the gastrointestinal tract and produce the toxin. Most infants show signs of constipation, followed by neuromuscular weakness that results in decreased sucking, lack of muscle tone and characteristic "floppy head." Symptoms may range from mild to severe, and may lead to respiratory failure.

Diagnosis

Physicians should consider a diagnosis of botulism in a patient who presents with neuromuscular impairment, but remains mentally alert. The disease is often mistaken for other more common conditions, including stroke, encephalitis, Guillain-Barré syndrome, myasthenia gravis, tick paralysis, chemical or mushroom poisoning, and adverse reactions to antibiotics or other medication. Sepsis, electrolyte imbalances, Reye syndrome, congenital myopathy, Werdnig-Hoffman disease and Leigh disease should be considered in infants.

A definitive diagnosis can be made by detecting the toxin in serum samples, or isolating C. botulinum from stool or wound specimens. Toxins can be detected with a mouse neutralization assay, or using PCR or ELISA protocols.

Treatment

Because of the threat of respiratory complications, patients should be hospitalized immediately and closely monitored. Mechanical ventilation should begin when the vital capacity falls below 30% of predicted. Trivalent (types A, B and E) equine antitoxin should be administered as soon as botulism is suspected to slow the progression of the illness and limit the duration of respiratory failure in critical cases. Caution should be exercised as approximately 9% of patients experience a hypersensitivity reaction. Due to the high incidence of side effects and anaphylaxis, infants should not receive equine antitoxin.

In 2003, the FDA approved an intravenously administered human botulism immune globulin for types A and B infant botulism.

Patients suffering from wound botulism should receive equine antitoxin and antibiotics such as penicillin.

Clinical Trials

As of early 2004, there was one open clinical trial for infant botulism at the National Institutes of Health (NIH), to assess the safety and efficacy of human botulism immune globulin.

Prognosis

Prompt diagnosis and treatment coupled with improved respiratory care have decreased mortality from food-borne botulism. Severe cases often call for prolonged respiratory support. The case-fatality rate is 7.5%, although mortality is greater in patients older than 60 years. Infant botulism has an excellent prognosis, although relapse can occur following hospital discharge. The case-fatality rate for infant botulism is 2%. Because toxin binding is irreversible, acetylocholine release and strength return only after the nerve terminals sprout new endings.

Resources

BOOKS

Ashbury, A. K., G. M. McKhann, W. I. McDonald, et al., eds. Diseases of the Nervous System: Clinical Neuroscience and Therapeutic Principles, Third Edition. Cambridge University Press, 2002.

Ford, M. D., D. A. Delaney, L. J. Ling, and T. Erickson, eds. Clinical Toxicology. New York: W. B. Saunders Company, 2001.

PERIODICALS

Cox, M., and R. Hinkle. "Infant Botulism." American Family Physician 65 (April 1, 2002): 1388-92.

Shapiro, R. L., C. Hatheway, and D. L. Swerdlow. "Botulism in the United States: A Clinical and Epidemiologic Review." Annals of Internal Medicine 129 (August 1988): 221-228.

OTHER

Abrutyn, Elias. "Chapter 144: Botulism." Harrison's Online. McGraw Hill, 2001. http://www.harrisonsonoline.com.

"Gastroenteritis Topics: Botulism," Section 3, chapter 28. In The Merck Manual of Diagnosis and Therapy, edited by TK. Merck & Co. Inc. 2004. http://www.merck.com.

World Health Organization. Botulism. Fact Sheet No. 270. http://www.who.int/mediacentre/facsheets/who270.html.

Hannah M. Hoag, MSc

An illness produced by the exotoxin of Clostridium botulinum and occasionally other clostridia, and characterized by paralysis and other neurological abnormalities. There are seven principal toxin types involved (A–G); only types A, B, E, and F have been implicated in human disease. Types C and D produce illness in birds and mammals. Strains of C. barati and C. butyricum have been found to produce toxins E and F and have been implicated in infant botulism. See also Virulence.

The three clinical forms of botulism are classic botulism, infant botulism, and wound botulism. Classic botulism is typically due to ingestion of preformed toxin, infant botulism involves ingestion of C. botulinum spores with subsequent germination and toxin production in the gastrointestinal tract, and wound botulism involves production of toxin by the organism's infecting or colonizing a wound. The incubation period is from a few hours to more than a week (but usually 1–2 days), depending primarily on the amount of toxin ingested or absorbed.

There is classically acute onset of bilateral cranial nerve impairment and subsequent symmetrical descending paralysis or weakness. Commonly noted are dysphagia (difficulty in swallowing), dry mouth, diplopia (double vision), dysarthria (a neuromuscular disorder affecting speech), and blurred vision. Nausea, vomiting, and fatigue are common as well. Ileus (impaired intestinal motility) and constipation are much more typical than diarrhea; there may also be urinary retention and dry mucous membranes. Central nervous system function and sensation remain intact, and fever does not occur in the absence of complications. Fever may even be absent in wound botulism. See also Toxin.

In food-borne botulism, home-canned or home-processed foods (particularly vegetables) are commonly implicated, with commercially canned foods involved infrequently. Outbreaks usually involve only one or two people, but may affect dozens. In infant botulism, honey and corn syrup have been implicated as vehicles. Therapy involves measures to rid the body of unabsorbed toxin, neutralization of unfixed toxin by antitoxin, and adequate intensive care support. See also Food poisoning; Poison.

A rare form of food poisoning caused by the extremely potent neurotoxins produced by Clostridium botulinum (isolated in 1895 by Belgian bacteriologist Emilie Pierre-Marie van Ermengem). At least seven different toxins have been identified; they can be inactivated by heating at 80 °C for 10 min., but in foods are more resistant to heat. Although rare, it is often fatal unless the antitoxin is given.

The name is derived from botulus, for sausage, since the disease was originally associated with sausages in Germany (the first recorded outbreak was in 1735). A wide range of foods have been involved, including meat, fish, milk, fruits, and vegetables which have been incorrectly preserved or treated, so that competing micro-organisms have been destroyed; spores of C. botulinum are extremely resistant to heat, and dangerous amounts of toxins can accumulate in contaminated foods without any apparent spoilage.

A particularly dangerous form of food poisoning caused by a toxin produced by the bacterium Clostridium botulinum. The bacterium is common in soil but also thrives in improperly processed foods, especially low-acid canned goods. Extra care should be taken to destroy bacteria during home-bottling. The toxin affects the central nervous system, particularly the cardiac and respiratory centres, and can cause death due to heart and lung failure. The toxin is usually destroyed during cooking.

One authoritative medical book recommends that infants under a year old should not be given home-made honey because it may contain dormant spores of Clostridium botulinum which can grow in the immature digestive tract. Honey is safe for older people because it does not contain the toxin and the bacterium cannot survive in the more mature gut.

Definition

Botulism is an acute, progressive condition caused by botulinum toxin, a natural poison produced by the spore-forming bacteria Clostridium botulinum. Exposure to the botulinum toxin usually occurs from eating contaminated food although, in infants, it may be caused by specific types of clostridia obtained from soil or inhaled spores, causing growth of the bacteria in the infant's intestine. Botulinum toxin is a neurotoxin that blocks the ability of motor nerves to release acetylcholine, the neurotransmitter that relays nerve signals to muscles, a process that may result in unresponsive muscles, a condition known as flaccid paralysis. Breathing may be severely compromised in progressive botulism because of failure of the muscles that control the airway and breathing.

Description

Botulism occurs only rarely, but its high fatality rate makes it a great concern for those in the general public and in the medical community. Clinical descriptions of botulism reach as far back in history as ancient Rome and Greece. However, the relationship between contaminated food and botulism was not defined until the late 1700s. In 1793 the German physician, Justinius Kerner (1786–1862), deduced that a substance in spoiled sausages, which he called wurstgift (German for sausage poison), caused botulism. The toxin's origin and identity remained vague until Emile van Ermengem (1851–1932), a Belgian professor, isolated Clostridium botulinum in 1895 and identified it as the source of food poisoning.

Three types of botulism have been identified: food-borne, wound, and infant botulism. The main difference between types hinges on the route of exposure to the toxin. Food-borne botulism accounts for 25 percent of all botulism cases and can usually be traced to eating contaminated home-preserved food. Infant botulism accounts for 72 percent of all cases. About 98 percent of infants recover with proper treatment. Although domestic food poisoning is a problem worldwide, concern is growing regarding the use of botulism toxin in biological warfare. At the end of the twentieth century 17 countries were known to be developing biological weapons, including the culture of botulism toxins.

Transmission

Botulism is not spread from one individual to another, but through exposure to the deadly botulinum toxin, a natural poison produced by certain Clostridium bacteria that may be found in preserved, especially canned, foods and sometimes in the intestines of infants. Botulism spores can cause widespread illness if introduced into the environment.

Demographics

Botulism occurs worldwide, with 90 percent of the comparatively rare cases occurring in the United States. Approximately 110 cases of botulism are reported annually in the United States, with 50 percent of cases in California alone. Infant botulism accounts for 72 percent of all cases, far exceeding both food-borne and wound botulism. Food-borne botulism accounts for 25 percent of all cases, primarily due to eating contaminated home-preserved food.

Causes and Symptoms

Toxins produced by the bacterium Clostridium botulinum are the main culprit in botulism. Other members of the Clostridium genus can produce botulinum toxin, namely C. argentinense, C. butyricum, and C. baratii, but these are minor sources. To grow, these bacteria require a low-acid, oxygen-free environment that is warm (40–120°F or 4.4–48.8°C) and moist. Lacking these conditions, the bacteria transform themselves into spores that, like plant seeds, can remain dormant for years. Clostridia and their spores exist all over the world, especially in soil and aquatic sediments. They do not threaten human or animal health until the spores encounter an environment that favors growth. The spores then germinate, and the growing bacteria produce the deadly botulism toxin.

Scientists have discovered that clostridia can produce at least seven types of botulism toxin, identified as A, B, C, D, E, F, and G. Humans are usually affected by A, B, E, and very rarely F; infants are affected by types A and B. Domesticated animals such as dogs, cattle, and mink are affected by botulism C toxin, which also affects birds and has caused massive die-offs in domestic bird flocks and wild waterfowl. Botulism D toxin can cause illness in cattle, and horses succumb to botulism A, B, and C toxin. There have been no confirmed cases of human or animal botulism linked to the G toxin.

In humans, botulinum toxin latches onto specific proteins in nerve endings and irreversibly destroys them. These proteins control the release of acetylcholine, a neurotransmitter that stimulates muscle cells. With acetylcholine release blocked, nerves are not able to stimulate muscles. Ironically, this action of the botulinum toxin has given it a beneficial niche in the world of medicine. Certain medical disorders are characterized by involuntary and uncontrollable muscle contractions. Medical researchers have discovered that injecting a strictly controlled dose of botulinum toxin into affected muscles inhibits excessive muscle contractions. The muscle is partially paralyzed and normal movement is retained.

Human botulism (caused by botulism toxins A, B, and E) may stem from contaminated food, wound contamination, or the intestinal botulism toxin found in infants. Each produces multiple symptoms as follows:

• Food-borne botulism. Food that has been improperly preserved or stored can harbor botulinum toxin-producing clostridia. Canned or jarred baby food has also been known to cause botulism. Symptoms of food-borne botulism typically appear within 18 to 36 hours of eating contaminated food, with extremes of four hours to eight days. Initial symptoms include blurred or double vision and difficulty swallowing and speaking. Possible gastrointestinal problems include constipation, nausea, and vomiting. As botulism progresses, the victim experiences weakness or paralysis, starting with the head muscles and progressing down the body. Breathing becomes increasingly difficult. Without medical care, respiratory failure and death are very likely.
• Infant botulism. Infant botulism was first described in 1976. Unlike adults, infants younger than 12 months are vulnerable to C. botulinum colonizing the intestine. Infants ingest spores in honey or simply by swallowing spore-containing dust or dirt. The spores germinate in the large intestine and, once colonized, toxin is produced and absorbed into the infant's body from the entire intestinal tract. The first symptoms include constipation, lethargy, and poor feeding. As infant botulism progresses, sucking and swallowing (thus eating) become difficult. A nursing mother will often notice her own breast engorgement as the first sign of her infant's illness. The baby suffers overall weakness and cannot control head movements. Because of the flaccid paralysis of the muscles, the baby appears floppy. Breathing is impaired, and death from respiratory failure is a very real danger.
• Wound botulism. Confirmed cases of wound botulism have been linked to trauma such as severe crush injuries to the extremities, surgery, and illegal drug use. Wound botulism occurs when Clostridia colonize an infected wound and produce botulinum toxin. The symptoms usually appear four to 18 days after an injury occurs and are similar to food-borne botulism, although gastrointestinal symptoms may be absent.

When to Call the Doctor

Infant botulism may be hard for parents to identify because the symptoms occur slowly. Parents should call the doctor or take the infant or child to emergency services as soon as the child shows symptoms such as weakness or listlessness, lethargy, irritability, and poor eating (or nursing) along with decreased bowel movements or constipation. An affected child may be so weak as to appear floppy and not in control of muscle movements, especially movement of the neck and head. Whether parents are aware of a possible source of the botulism toxin, the suggestive symptoms should not be ignored.

Diagnosis

Differential diagnosis of botulism can be complex because the symptoms mimic those of other diseases, especially diseases characterized by muscle weakness. Botulism must be differentiated from diseases such as the following:

• Guillain-Barré syndrome
• meningoencephalitis
• myasthenia gravis
• systemic poisoning or sepsis
• reactions to therapeutic drugs
• nervous system infection
• carbon monoxide or atropine intoxication
• severe allergic reactions to bee sting, shell fish, and other allergens
• failure to thrive

Sepsis is the most common initial diagnosis for actual infant botulism, and meningoencephalitis may also be the diagnosis if irritability and lethargy are present. Infant botulism was at one time linked to 5 to 15 percent of cases of sudden infant death syndrome (SIDS, crib death) because of spores found in 4 to 15 percent of cases; however, a subsequent 10-year study did not find a significant influence of botulism on SIDS.

Laboratory tests are used to make a definitive diagnosis, but if botulism seems likely, treatment starts immediately without waiting for test results, which may take up to two days. Diagnostic tests focus on identifying the organism causing the illness. This may involve performing a culture on contaminated material from the suspect food or the nose or throat of the affected individual. In infant botulism, the infant's stool may be cultured to isolate the organism; this test may be performed by the state health department or the Centers for Disease Control (CDC). Culture results are available from the microbiology laboratory as soon as bacteria grow in a special plate incubated at temperatures at or above body temperature. The growth of Clostridium confirms the diagnosis. Sometimes the organism cultured is not Clostridium as suspected. The microbiology laboratory may use samples of the bacteria grown to perform other special techniques in order to help identify the causative organism.

While waiting for diagnostic test results, doctors ask about recently consumed food, possible open sores, recent activities and behavior, and other factors that may help to rule out other disease possibilities. A physical examination is done with an emphasis on the nervous system and muscle function. As part of this examination, imaging studies such as CT and MRI may be done and electrodiagnostic muscle function tests (electromyogram) or lumbar punctures may be ordered. Laboratory tests look for the presence of botulinum toxin or Clostridia in suspected foods and/or the child's blood serum, feces, or other specimens for traces of botulinum toxin or Clostridia. Magnesium levels may be measured, since magnesium increases the activity of Clostridium. Additional diagnostic tests may be done to rule out other diseases or conditions with similar symptoms.

Treatment

Drugs

Older children and adults with botulism are sometimes treated with an antitoxin derived from horse serum that is distributed by the Centers for Disease Control and Prevention. The antitoxin (effective against toxin types A, B, and E) inactivates only the botulinum toxin that is unattached to nerve endings. Early injection of the antitoxin, ideally within 24 hours of onset of symptoms, can preserve nerve endings, prevent progression of the disease, and reduce mortality.

Unfortunately, infants cannot receive the antitoxin used for adults. For them, human botulism immune globulin (BIG) is the preferred treatment. It is available in the United States through the Infant Botulism Treatment and Prevention Program in Berkeley, California. BIG neutralizes toxin types A, B, C, D, and E before they can bind to nerves. This antitoxin can provide protection against A and B toxins for approximately four months. Though many infants recover with supportive care, BIG cuts hospital stay in half and, therefore, reduces hospital costs by 50 percent as well.

Aside from the specific antitoxin, no therapeutic drugs are used to treat botulism. Antibiotics are not effective for preventing or treating botulism because the Clostridium group of toxins are not sensitive to them. In fact, antibiotic use is discouraged for infants because bacteria could potentially release more toxin into a baby's system as they are killed. Antibiotics can be used, however, to treat secondary respiratory tract and other infections.

Respiratory Support

Treatment for infants usually requires them to be in an intensive care unit, involving intensive respiratory support and nasogastric tube feeding for weeks or even months. Once an infant can breathe unaided, physical therapy is initiated to help the child relearn how to suck and swallow. In older children and adults, a respirator is often required to assist breathing; a tracheostomy may be necessary in some cases.

Surgery

Surgery may be necessary to clean an infected wound (debridement) and remove the source of the bacteria producing the toxin. Antimicrobial therapy may be necessary.

Gastric Lavage

When botulism in older children or adults is caused by food, it often is necessary to flush the gastrointestinal tract (gastric lavage). Often cathartic agents or enemas are used. It is important to avoid products that contain magnesium, since magnesium enhances the effect of the toxin.

Nutritional Concerns

Parents should avoid feeding honey to infants younger than 12 months because it is one known source of botulism spores.

Prognosis

With medical intervention, botulism victims can recover completely, though it may be a very slow recovery. It takes weeks to months to recover from botulism, and severe cases can take years before a total recovery is attained. Recovery depends on the nerve endings building new proteins to replace those destroyed by botulinum toxin.

Prevention

Vaccines have not been developed directed against botulism, which makes prevention of infant botulism or other forms of the disease difficult, since exposure to the botulinum toxic is typically unrecognized. Food safety is the surest prevention for botulism. Botulinum toxin cannot be seen, smelled, or tasted, so the wisest course is to discard any food that seems spoiled; avoid eating food from dented, rusty, or bulging cans; avoid refreezing meats once they have been thawed; and avoid buying broken containers of food or eating food that has been stored at room temperature or above for more than a few hours. People who like to can food at home must be diligent about using sterile equipment and following U.S. Department of Agriculture canning guidelines.

Infant botulism is difficult to prevent, because controlling what goes into an infant's mouth is often beyond control, especially in regard to airborne spores. One concrete preventative is to never feed honey to infants younger than 12 months as it is one known source of botulism spores. As infants begin eating solid foods, the same food precautions should be followed as for older children and adults.

Parental Concerns

Because symptoms of infant botulism appear slowly, parents may be concerned that they will be missed or not found early. Normal watchfulness of the parents is sufficient, paying attention to any change in feeding, a decrease in bowel movements, or a lack of normal responses such as turning of the head and body movements. It may be helpful to remember how rare botulism is, how easy it is to assure food safety, and also that morbidity and mortality can be avoided with early recognition of the symptoms.

Resources

Books

Rosaler, Maxine. Botulism. New York: Rosen Publishing Group, 2004.

Periodicals

Cadou, Stephanie G. "Diagnosing Infant Botulism." The Nurse Practitioner 26, no. 3 (March 2001): 76.

Organizations

Centers for Disease Control and Prevention. 1600 Clifton Rd., NE, Atlanta, GA 30333. Web site: www.cdc.gov.

[Article by: L. Lee Culvert Janie F. Franz]

Botulism is a rare disease that occurs in four forms: food-borne botulism (the most common form); infant botulism (sometimes associated with honey); an adult form of infant botulism; and wound infection botulism. Botulism is caused by botulinum neurotoxin, which blocks acetylcholine release at neuromuscular junctions, resulting in paralysis. The toxin is produced under anaerobic conditions by Clostridium botulinum, a bacterium found widely in the environment.

In food-borne botulism, the preformed toxin is ingested. There are two main bacterial strains: Group I strains are proteolytic, have spores that are highly resistant to heat, and cannot grow below 10°C. Group II strains are nonproteolytic, are less likely to survive thermal processing or grow in acid or salty products, and grow at refrigeration temperatures. The canning industry has developed retort conditions to prevent the survival of all spores.

Symptoms of food-borne botulism include double vision, inability to speak or swallow, labored breathing, and death. Food-borne botulism can be caused by improperly processed or stored foods, including vegetables, meat, fish, and cheese. The annual incidence of botulism is highest in Russia, Poland, and Hungary with 0.2 to 0.3 cases per 100,000 persons (due to contaminated home-preserved foods); and in the Innuit populations of Canada and Alaska (60 cases per 100,000 persons in northern Quebec), where it is usually associated with toxins in putrefied whale, seal, or fish products.

Symptoms of infant botulism include constipation, weakness, and respiratory arrests, but rarely death.

(SEE ALSO: Food-Borne Diseases)

Bibliography

Austin, J. W., and Dodds, K. L. (2001). "Clostridium botulinum." In Food-borne Disease Handbook, 2nd edition, eds. Y. H. Hui, M. D. Pierson, and J. R. Gorham. New York: Marcel Dekker.

Center for Food Safety and Applied Nutrition. Clostridium botulinum. In Bad Bug Book (Food-borne Pathogenic Microorganisms and Natural Toxins Handbook). Washington, DC: Center for Food Safety and Applied Nutrition U.S. Food and Drug Administration. Available at http://vm.cfsan.fda.gov/~mow/chap2.html.

— EWEN TODD

For more information on botulism, visit Britannica.com.

Botulism is a paralytic illness caused by a nerve toxin produced by the soil bacterium Clostridium botulinum and spread by contaminated food or by infection of a wound. The term comes from the Latin botulus (sausage), but the vehicle in food-borne cases today is usually vegetables or other food improperly canned at home. Commercial canning is almost never implicated, although a notable case in 1971 left one person dead and several others seriously injured. The illness is rare, with only twenty-five to thirty food-borne cases reported annually in the United States.

C. botulinum is a spore-forming bacteria that can lie dormant in the soil for months or years. In a warm, moist, low-oxygen environment, however, the spores can produce vegetative cells that multiply rapidly and secrete a deadly toxin, which attacks the nervous system of the person ingesting contaminated food.

Symptoms of botulism include double vision, blurred vision, drooping eyelids, slurred speech, difficulty in swallowing, dry mouth, and muscle weakness. An antitoxin can be used with early diagnosis, but otherwise treatment involves supportive care, sometimes including a ventilator. A severe case can require months of medical and nursing care and may leave the patient with permanent impairments. Botulism is fatal in about 8 percent of cases, usually from respiratory failure.

Thorough washing can remove the spores and proper heating will destroy them. If, however, the food being canned is not washed properly and fails to reach the necessary temperature for the required time, the spores can germinate and produce toxin in the canned goods.

A pH in the acid range will also kill the spores, so acidic foods such as fruit and tomatoes are less likely to be vehicles than low-acid food such as corn, green beans, or asparagus. Canners are often advised to raise the acidity of food by adding an acid source such as lemon juice or citric acid.

To avoid the danger of botulism, home canners of low-acid foods are advised to use a pressure canner instead of the unpressurized, boiling-water-bath systems used previously. A temperature of up to 250°F is needed, which can be reached with pressure canners operated at ten to fifteen pounds per square inch. The time required ranges from twenty to one hundred minutes, depending on the food and the size of the jars. Detailed instructions are available with home canning systems, either from the U.S. Department of Agriculture or from an extension agent.

Industrial quality control makes it highly unlikely that commercially canned food will be contaminated with botulinum toxin. However, consumers should reject any commercial canned goods that appear swollen or bulging and any canned food with a bad smell or flavor.

In recent years, scientists have recognized an infant form of botulism in which infants ingest spores that germinate and produce toxins in the intestines. This appears to be linked mainly to the ingestion of raw honey, so authorities urge parents never to feed raw honey to babies. There is little danger of this variant of the disease after the age of one year.

Bibliography

Centers for Disease Control and Prevention. "Botulism." At http://www.cdc.gov/health/botulism.htm.

Silliker, J. H., ed. Microbial Ecology of Foods. Vol. 1. New York: Academic Press, 1980.

U.S. Department of Agriculture. Complete Guide to Home Canning. Washington, D.C., 1994.

—Richard L. Lobb

A severe form of food poisoning, often fatal if not treated quickly. Botulism is caused by a kind of bacterium that produces a toxin, and it is sometimes present in improperly canned or preserved foods.

A highly fatal toxemia caused by the ingestion of toxin produced during vegetative growth of Clostridium botulinum in decomposing animal matter. In agricultural animals, ingestion of preformed toxin most commonly results from contamination during feed preparation or storage allows multiplication of the organism in the feed or allows contamination of feed with carrion containing toxin. In companion animals it occurs as the result of feeding on carrion. The clinical picture includes the development of flaccid paralysis over a period of 1 to 3 days, the animal becoming recumbent and being unable to eat or drink, but being fully conscious. Death is caused by respiratory paralysis. Called also western duck disease, limberneck.

• wound b. — a form resulting from infection of a wound with Clostridium botulinum. Called also toxicoinfectious botulism.
• toxicoinfectious b. — growth and toxin production of the organism in the alimentary tract.

The botulinum toxin is extremely lethal and easy to produce. A small quantity of this toxin can destroy the central nervous system. Botulism may be contracted by eating contaminated foods or by absorbing the bacteria through cuts in the skin. Fewer than 200 cases reported annually in the U.S. Intentional contamination of the food supply or aerosol dissemination of the toxin is the greatest concern of counterterrorists.

Botulism (Latin, botulus, "sausage") also known as botulinus intoxication is a rare but serious paralytic illness caused by botulinum toxin, which is produced by the bacterium Clostridium botulinum. The toxin enters the body in one of four ways: by colonization of the digestive tract by the bacterium in children (infant botulism) or adults (adult intestinal toxemia), by ingestion of toxin from foodstuffs (foodborne botulism) or by contamination of a wound by the bacterium (wound botulism).^[1] All forms lead to paralysis that typically starts with the muscles of the face and then spreads towards the limbs.^[1] In severe forms, it leads to paralysis of the breathing muscles and causes respiratory failure. In view of this life-threatening complication, all suspected cases of botulism are treated as medical emergencies, and public health officials are usually involved to prevent further cases from the same source.^[1]

Contents 1 Signs and symptoms 1.1 Clinical features 1.2 Mode of acquisition 1.3 Infant botulism 1.4 Complications 2 Mechanism 3 Diagnosis 4 Prevention 5 Treatment 6 Prognosis 7 Epidemiology 8 See also 9 References 10 External links

Signs and symptoms

Clinical features

The muscle weakness of botulism characteristically starts in the muscles supplied by the cranial nerves. This group of twelve nerves controls eye movements, the facial muscles and the muscles controlling chewing and swallowing. Double vision, drooping of both eyelids, loss of facial expression and swallowing problems may therefore occur, as well as difficulty with talking. The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet).^[1] Severe botulism leads to reduced movement of the muscles of respiration, and hence problems with gas exchange. This may be experienced as dyspnea (breathlessness), but when severe can lead to respiratory failure: to the buildup of unexhaled carbon dioxide and its resultant depressant effect on the brain. This may lead to coma and eventually death if untreated.^[1]

In addition to affecting the voluntary muscles, it can also cause disruptions in the autonomic nervous system. This is experienced as a a dry mouth and throat (due to decreased production of saliva), postural hypotension (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually constipation (due to decreased peristalsis).^[1] Some of the toxins (B and E) also precipitate nausea and vomiting.^[1]

Mode of acquisition

Four main modes of entry for the toxin are known. The most common form in Western countries is infant botulism. This occurs in small children who are colonized with the bacterium during the early stages of their life. The bacterium then releases the toxin into the intestine, which is absorbed into the bloodstream. While the consumption of honey during the first year of life has been identified as a risk factor for infant botulism, it is only a factor in a fifth of all cases.^[1] The adult form of infant botulism is termed adult intestinal toxemia, and is exceedingly rare.^[1]

Foodborne botulism results from contaminated foodstuffs in which C. botulinum spores have been allowed to germinate. This typically occurs in home-canned food substances and fermented uncooked dishes. Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. It takes 3–5 days for the symptoms to become apparent.^[1]

Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins.^[1]

Isolated cases of botulism have been described after inhalation by laboratory workers and after cosmetic use of inappropriate strengths of Botox.^[1]

Infant botulism

Infant botulism (first recognized in 1976) is the most common form of the ailment in the United States. It affects about 100 infants per year in the United States. Infants less than 12 months of age are susceptible, with almost 90% of cases occurring between the ages of 3 weeks and 6 months of age at presentation. The mode of action of this form is through colonization by germinating spores in the gut of an infant. The first symptom is usually constipation, followed by generalized weakness, loss of head control and difficulty feeding. Like the other forms of botulism, the symptoms are caused by the absorption of botulinum toxin, and typically progress to a symmetric descending flaccid paralysis. Death is often the eventual outcome unless the infant receives artificial ventilation.

Sweeteners such as honey and aspartame 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 microflora in their intestines to competitively exclude C. botulinum. Unopposed in the small intestine, the warm body temperature 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 no sweetener be given to children until after 12 months. Nevertheless, the majority of infants with botulism have no dietary history, 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.

Complications

Botulism can result in death due to respiratory failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 8% due to improved supportive care. A patient with severe botulism may require a breathing machine as well as intensive medical and nursing care for several months. Patients who survive an episode of botulism poisoning may have fatigue and shortness of breath for years and long-term therapy may be needed to aid their recovery.

Infant botulism has no long-term side effects, but can be complicated by nosocomial adverse events. The case fatality rate is less than 1% for hospitalized infants with botulism.

Mechanism

C. botulinum is an anaerobic, Gram positive, spore-forming rod. Botulin toxin is one of the most powerful known toxins: about one microgram is lethal to humans. It acts by blocking nerve function and leads to respiratory and musculoskeletal paralysis.

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.^[2] Specifically, the inhibition of the release of Acetylcholine from motor neurons, which synapse with the myofibers at the neuro muscular junction, results in a loss of muscle function, and paralysis.

Diagnosis

Physicians may consider diagnosing botulism if the patient's history and physical examination suggest botulism. However, these clues are often not enough to allow a diagnosis. Other diseases such as Guillain-Barré syndrome, stroke, and myasthenia gravis can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an Edrophonium Chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the feed, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony.^[3]

In cattle, the symptoms may include drooling, restlessness, uncoordination, 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 paralyzed 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.^[4]

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 diarrhea with excess urates.

Prevention

While commercially canned goods are required to undergo a "botulinum cook" at 121 °C (250 °F) for 3 minutes, and so rarely cause botulism, there have been notable exceptions such as the 1978 Alaskan salmon outbreak and the 2007 Castleberry's Food Co. outbreak. Foodborne botulism has more frequently been from home-canned foods with low acid content, such as carrot juice, asparagus, green beans, beets, and corn. However, outbreaks of botulism have resulted from more unusual sources. In July, 2002, fourteen Alaskans ate muktuk (whale meat) from a beached whale, and eight of them developed symptoms of botulism, two of them requiring mechanical ventilation^[5]. Other sources of infection include garlic or herbs^[6] stored covered in oil without acidification,^[7] chile peppers,^{[citation needed]} improperly handled baked potatoes wrapped in aluminium foil ^[8], and home-canned or fermented fish. Persons who do home canning should follow strict hygienic procedures to reduce contamination of foods. Oils infused with garlic or herbs should be refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated ^[8]. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 20 minutes before eating. Metal cans containing food in which bacteria, possibly botulinum, are growing may bulge outwards due to gas production from bacterial growth; such cans should be discarded. Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should also be discarded.

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.

Treatment

The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a ventilator for weeks, plus intensive medical and nursing care. After several weeks, the paralysis slowly improves. If diagnosed early, foodborne and wound botulism can be treated by inducing passive immunity with a horse-derived antitoxin, which blocks the action of toxin circulating in the blood.^[9] This can prevent patients from worsening, but recovery still takes many weeks. Physicians may try to remove contaminated food still in the gut by inducing vomiting or by using enemas. Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism.

Besides supportive care, infant botulism can be treated with botulism immunoglobulin intravenously (BIG-IV),(source Microbiology 2nd edition baumen 2009) 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.^[10]

Prognosis

This article may be confusing or unclear to readers. Please help clarify the article; suggestions may be found on the talk page. (February 2009)

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 are 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%.

Death from botulism is common in waterfowl; an estimated 10 to 100 thousand birds die of botulism 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 domestic mammals; however, in some parts of the world, epidemics with up to 65% mortality are seen in cattle. The prognosis is poor in large animals that are recumbent. Most dogs with botulism recover within 2 weeks.

Epidemiology

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 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.^[11]

See also

• List of foodborne illness outbreaks
• Botox
• Centers for Disease Control and Prevention (CDC)
• Castleberry's Food Company

References

1. ^ ^{a b c d e f g h i j k l} Sobel J (October 2005). "Botulism". Clin. Infect. Dis. 41 (8): 1167–73. doi:10.1086/444507. PMID 16163636. 
2. ^ Oxford Textbook of Medicine, 4th Ed., Section 7.55
3. ^ Weber,J.T. "Botulism" In Infectious Diseases, 5th ed. Edited by P.D. Hpeprich, J.B. Lippincott Company, 1994, pp. 1185-1194.
4. ^ "Botulism." In the Merck Veterinary Manual, 8th ed. Edited by S.E. Aiello and A. Mays. Whitehouse Station, NJ: Merck and CO., 1988, pp.442-444.
5. ^ "Outbreak of botulism type E associated with eating a beached whale--Western Alaska, July 2002". MMWR Morb. Mortal. Wkly. Rep. 52 (2): 24–6. January 2003. PMID 12608715. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5202a2.htm. 
6. ^ Oil Infusions and the Risk of Botulism, Colorado State University Cooperative Extension, Safefood new - Summer 1998 - Vol 2 / No. 4
7. ^ "Update: international outbreak of restaurant-associated botulism--Vancouver, British Columbia, Canada". MMWR Morb. Mortal. Wkly. Rep. 34 (41): 643. October 1985. PMID 3930945. http://www.cdc.gov/mmwr/preview/mmwrhtml/00000627.htm. 
8. ^ ^{a b} "Botulism Linked to Baked Potatoes". http://www.personalmd.com/news/a1998062515.shtml. Retrieved on 2007-03-21. 
9. ^ Shapiro RL, Hatheway C, Swerdlow DL (August 1998). "Botulism in the United States: a clinical and epidemiologic review". Ann. Intern. Med. 129 (3): 221–8. PMID 9696731. 
10. ^ http://mmrs.fema.gov/news/publichealth/2006/aug/nph2006-08-03a.aspx^{[broken citation]}
11. ^ Passaro DJ, Werner SB, McGee J, Mac Kenzie WR, Vugia DJ (March 1998). "Wound botulism associated with black tar heroin among injecting drug users". JAMA 279 (11): 859–63. doi:10.1001/jama.279.11.859. PMID 9516001. 

External links

• Agent Fact Sheet: Botulism, Center for Biosecurity
• Botulism (Technical information from the CDC)
• Infant Botulism Treatment and Prevention Program
• Clostridium Botulinum (FDA/CFSAN)
• Botulism (WHO)
• Avian Botulism

v • d • e Infectious diseases · Bacterial diseases: G+ (primarily A00-A79, 001-041,080-109) Firmicutes/ (low-G+C) Bacilli Lactobacillales (Cat-) Streptococcus Alpha hemolytic optochin susceptible: S. pneumoniae (Pneumococcal infection) optochin resistant: S. viridans (S. mitis, S. mutans, S. oralis, S. sanguinis, S. sobrinus, milleri group) Beta hemolytic A, bacitracin susceptible: S. pyogenes (Scarlet fever, Erysipelas, Rheumatic fever, Streptococcal pharyngitis) B, bacitracin resistant, CAMP test+: S. agalactiae Gamma hemolytic D, BEA+: Streptococcus bovis Enterococcus BEA+: Enterococcus faecalis (Urinary tract infection) · Enterococcus faecium Bacillales (Cat+) Staphylococcus Cg+ S. aureus (Staphylococcal scalded skin syndrome, Toxic shock syndrome) Cg- novobiocin susceptible (S. epidermidis) · novobiocin resistant (S. saprophyticus) Bacillus Bacillus anthracis (Anthrax) · Bacillus cereus (Food poisoning) Listeria Listeria monocytogenes (Listeriosis) Clostridia Clostridium (spore-forming) motile: Clostridium difficile (Pseudomembranous colitis) · Clostridium botulinum (Botulism) · Clostridium tetani (Tetanus) nonmotile: Clostridium perfringens (Gas gangrene, Clostridial necrotizing enteritis) Peptostreptococcus (non-spore forming) Peptostreptococcus magnus Mollicutes Mycoplasmataceae Ureaplasma urealyticum (Ureaplasma infection) · Mycoplasma genitalium · Mycoplasma pneumoniae (Mycoplasma pneumonia) Anaeroplasmatales Erysipelothrix rhusiopathiae (Erysipeloid) Actinobacteria/ (high-G+C) Actinomycineae Actinomycetaceae Actinomyces israelii (Actinomycosis/Actinomycetoma) · Tropheryma whipplei (Whipple's disease) Propionibacteriaceae Propionibacterium acnes Corynebacterineae Mycobacteriaceae M. tuberculosis/M. bovis Tuberculosis: Ghon focus/Ghon's complex · Pott disease · brain (Meningitis, Rich focus) · cutaneous (Scrofula, Bazin disease, Lupus vulgaris, Prosector's wart) · Miliary · Tuberculous pericarditis M. leprae Leprosy Nontuberculous R1: M. kansasii R3: M. avium complex (MAA, MAP, MAI, Lady Windermere syndrome) · M. ulcerans (Buruli ulcer) Nocardiaceae Nocardia asteroides/Nocardia brasiliensis (Nocardiosis, Maduromycosis, Mycetoma) · Rhodococcus equi Corynebacteriaceae Corynebacterium diphtheriae (Diphtheria) · Corynebacterium minutissimum (Erythrasma) · Corynebacterium jeikeium Bifidobacteriaceae Gardnerella vaginalis

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Dansk (Danish)
n. - botulisme, pølseforgiftning

Nederlands (Dutch)
botulisme, vleesvergiftiging

Français (French)
n. - botulisme

Deutsch (German)
n. - Botulismus, Fleischvergiftung

Ελληνική (Greek)
n. - (παθολ.) βοτυλίαση, αλλαντίαση

Italiano (Italian)
botulismo

Português (Portuguese)
n. - botulismo (m) (Med.)

Русский (Russian)
ботулизм

Español (Spanish)
n. - botulismo

Svenska (Swedish)
n. - botulism (magförgiftning)

中文（简体）(Chinese (Simplified))
香肠中毒, 肉毒杆菌毒素

中文（繁體）(Chinese (Traditional))
n. - 香腸中毒, 肉毒桿菌毒素

한국어 (Korean)
n. - (병)보툴리누스 중독

日本語 (Japanese)
n. - ボツリヌス中毒

العربيه (Arabic)
‏(الاسم) تسمم من طعام فاسد‏

עברית (Hebrew)
n. - ‮הרעלה ממזון‬

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