Botulism

• 1. Introduction

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  Botulism takes its name from the Latin word botulus, which means sausage. The illness is caused by botulinum toxin, and about one microgram of it is lethal to a human who inhales it. That makes it one of the most powerful toxins known. Yet the bacterium that makes it, Clostridium botulinum, is an ordinary resident of soil and water. Worldwide, roughly 1,000 cases are identified each year. This documentary follows an everyday microbe that produces an extreme poison. How does the toxin silence nerves, and why does paralysis begin in the face? Why do babies, home cooks and wild animals all fall to the same disease? And why did military planners decide to study it?

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• 2. Spores and Phages

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  Eight varieties of Clostridium botulinum are labelled with the letters A to H. The organism is a rod-shaped bacterium that thrives without oxygen and forms spores. A spore is a tough, dormant form that the cell makes when it is under stress.

  The toxin itself comes in types A through G. These differ in how the immune system recognizes them, yet they are similar in structure. Human botulism comes mainly from types A, B and E, and rarely from type F. Types C and D poison only other animals.

  In October 2013, scientists announced type H, the first new botulism neurotoxin found in forty years. Further study showed that it was a chimera, a hybrid built from parts of types F and A.

  The spores collect in soil and in the silt at the bottom of streams, lakes and coastal waters. Some types also live naturally in the intestines of mammals such as horses, cattle and humans. A spore can stay inert for many years, and boiling does not kill it.

  Warmth, moisture, a protein source and the absence of oxygen are what wake the spores and start toxin production. In food, a low-salt, low-acid, low-sugar setting at ambient temperature is also needed. Such conditions are rarely met, which is why botulism is uncommon.

  The gene for the toxin protein turns out to be carried by a virus, called a phage, that infects the bacterium. Little is known about what controls that infection and replication in nature.

  Types A, and some of B and F, digest meat and give off a putrefactive smell. Type E and some of B, C, D and F have no strong odor, so they can go undetected.

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• 3. Paralysis and Rescue

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  Twelve cranial nerves control eye movements, the facial muscles, chewing and swallowing, and botulism strikes the muscles they supply first. Double vision, drooping of both eyelids, loss of facial expression and trouble swallowing may follow. The toxin blocks the release of acetylcholine, the chemical messenger that tells a muscle to move, at the junction where nerve meets muscle. Types A and E cut a protein called SNAP-25. Types B, D, F and G cut synaptobrevin. Type C cuts both SNAP-25 and syntaxin. Nerves that fire most often are hit first, which shapes the pattern of damage.

  Types B and E also bring nausea, vomiting and difficulty talking. The autonomic nervous system, which runs functions beyond conscious control, falters as well. Saliva falls, leaving a dry mouth and throat. Blood pressure drops on standing, which risks lightheadedness and blackouts. Constipation follows as the gut slows.

  From the face, weakness moves to the arms, beginning at the shoulders and reaching the forearms. It then spreads to the legs, from the thighs down to the feet. In severe cases the breathing muscles move less, and unexhaled carbon dioxide builds up. Breathlessness comes first, and untreated respiratory failure can end in death.

  Clinicians often remember a classic triad of signs. These are paralysis descending from the nerves of the head, no fever, and a clear mind, known as a clear sensorium.

  Guillain-Barré syndrome, stroke and myasthenia gravis can look similar to botulism. Doctors may therefore order a brain scan, a spinal fluid examination, a nerve conduction test or the Tensilon test for myasthenia gravis. In babies, diagnosis rests on signs and symptoms, and a stool or enema specimen tested in mice confirms it. In others, a definite diagnosis comes when toxin is found in food, stomach or intestinal contents, vomit or feces. It is occasionally found in blood. Because breathing can fail, every suspected case is a medical emergency, and public health officials usually step in to trace the source.

  Without treatment, botulism is fatal in 40 to 50 percent of cases. Today five to ten percent of affected people die. Half a century ago roughly half of patients died, and improved supportive care has brought the figure down to 7 percent.

  Paralysis can last two to eight weeks, and a ventilator may be needed for that long, sometimes for months, with intensive nursing. Paralysis eases as new connections between nerve and muscle form. Many patients still have fatigue and breathing problems afterward, and some need rehabilitation.

  Botulism antitoxin is made of antibodies that neutralize toxin circulating in the blood. It stops more toxin from binding at the nerve-muscle junction, but it cannot undo paralysis already caused. In adults, a trivalent antitoxin against types A, B and E, derived from horses, is used most often. In the United States it is available from the local health department through the CDC. A heptavalent version, covering types A through G, was approved by the US FDA in 2013.

  For infants, doctors sometimes avoid horse-derived antitoxin for fear of serum sickness, an allergic reaction to horse proteins. A human-derived antitoxin was approved by the FDA in 2003 for infant botulism. Hospitalized babies have a case fatality rate below two percent. Other measures include inducing vomiting or giving enemas to clear food from the gut. Wounds are treated, usually surgically, to remove the source of the bacteria, and antibiotics may be used for wound botulism.

  A vaccine exists but is rarely used. In 2011 the US CDC discontinued it after the product lost potency and booster shots caused more moderate local reactions. As of 2017, work on a better vaccine continued, but the FDA had approved none.

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• 4. Honey, Wounds, and Needles

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  Infant botulism was first recognized in 1976, and it is now the most common form in the United States. It is also called floppy baby syndrome. More than 90 percent of cases occur in babies younger than six months.

  A baby swallows spores, and the bacterium then colonizes the small intestine. The infant's gut bacteria do not yet crowd it out. Bile acids, which normally hold clostridial growth in check, are also at lower levels than later in life. In older children and adults, normal intestinal bacteria suppress the organism.

  Constipation is usually the first sign of infant botulism, but it is often overlooked. Lethargy, weakness, trouble feeding and an altered cry can follow. The illness may progress to complete limp paralysis that starts at the head and moves downward.

  Honey is a known reservoir of the spores and is a factor in a fifth of all infant cases. For that reason, honey is not recommended for children under 12 months. Most cases, though, are thought to come from spores in the natural environment. Many affected babies lived near a construction site or an area of disturbed soil. Cases have been reported in 49 of 50 US states, all except Rhode Island, and in 26 countries on five continents. The adult counterpart, adult intestinal toxemia, is exceedingly rare.

  Since the 1990s, wound botulism has grown more common among people who inject drugs. It is especially linked to black tar heroin and to heroin injected into the skin rather than a vein. A minor wound can do the same if it is not cleaned properly. One person cut an ankle while using a weed eater. As the skin healed over, it trapped a blade of grass and a speck of soil. The result was severe botulism, with hospitalization and months of rehabilitation.

  Isolated cases have also been described in laboratory workers who inhaled the toxin.

  After a 2008 review, the US FDA added a boxed warning about botulinum toxin injections. Symptoms can appear away from the injection site, including weakness, blurred vision, a changed voice and trouble breathing, which can be fatal. Onset ranges from hours to weeks after the injection. The problem generally arises from inappropriate strengths for cosmetic use or from the larger doses used for movement disorders. NeverTox, an international grassroots group, runs a Facebook group of 39,000 people who believe they suffer adverse events from these injections.

  Before the warning labels, a series of lawsuits targeted the manufacturers. A Hollywood producer's wife sued after a migraine treatment. A suit for a 3-year-old boy who was permanently disabled was settled during trial. The family of a 7-year-old treated for leg spasms sued after he almost died. Several families of people who died brought suits too. One plaintiff, a physician diagnosed with botulism by thirteen neurologists at the NIH, was awarded $15 million. Deposition video from that case quotes a pharmaceutical executive saying, "Botox doesn't cause botulism."

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• 5. Rules of the Kitchen

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  A pH of 4.6 is the dividing line in home canning. Foods at 4.6 or below count as acid foods, including fruits, pickles, sauerkraut, jams, jellies, marmalades and fruit butters. Low-acid foods sit above that line. They include red meats, seafood, poultry, milk and all fresh vegetables except most tomatoes.

  Some tomatoes and figs have a pH slightly above 4.6. Lemon juice or citric acid must bring them down before canning. Mixtures of low-acid and acid foods also stay above 4.6 unless the recipe has enough lemon juice, citric acid or vinegar. For home preserves, only acidic fruit such as apples, pears, stone fruits and berries should be used on their own. Tropical fruit needs added acid.

  Home-canned carrot juice, asparagus, green beans, beets and corn have been common culprits, all low in acid. Fish pickled without enough salt and acid is a risk, and so is smoked fish stored too warm. Rarer sources, appearing about once a decade in the United States, include garlic or herbs stored in oil without acidification, chili peppers, tomatoes and fermented fish. Oils infused with fresh garlic or herbs should be acidified and refrigerated.

  The toxin is destroyed by heating above 85 degrees Celsius for more than five minutes. Spores survive that treatment and ordinary boiling. For this reason, home-canned foods are best boiled for 10 minutes before eating.

  A can that bulges outward from gas, holds foamy food or smells bad should be thrown away. So should any can with pinprick holes from rust or damage. Yet contamination with the bacterium alone may leave no visible defect, so a smooth can proves nothing. Only sufficient heat processing during production, and no route for later contamination, are reliable signs of safety.

  Commercial canning applies a "botulinum cook" in a pressure cooker at 121 degrees Celsius for 3 minutes. That is why factory cans rarely cause botulism. Processed meats get another safeguard. Nitrites and nitrates added to ham, bacon and sausages reduce growth and toxin production. Lactate and sorbate protect similarly but do not give the desirable pink color.

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• 6. Outbreaks Worldwide

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  Between the 31st of March and the 6th of April 1977-59 people in Pontiac, Michigan developed type B botulism. All had eaten at the same Mexican restaurant. The source was a hot sauce made with improperly home-canned jalapeño peppers, added to meals or served on nachos. Doctors documented the full range of type B illness, from mild symptoms to life-threatening paralysis of breathing.

  In April 1994, El Paso, Texas had the largest US outbreak since 1978. Thirty people fell ill, and four needed mechanical ventilation. All had eaten at one Greek restaurant. Of 22 diners who ate the potato-based dip, 19 became ill, an attack rate of 86 percent. Among those who skipped it, the rate was 6 percent. The eggplant-based dip showed 67 percent against 13 percent. Type A toxin turned up in patients and in both dips. Baked potatoes wrapped in aluminum foil had apparently sat at room temperature for several days before going into the dips.

  Factory cans have failed only rarely. One exception was a 1978 Alaskan salmon outbreak. Beginning in late June 2007, eight people were poisoned by canned food from Castleberry's Food Company in Augusta, Georgia. One line of industrial cooking vessels called retorts had under-processed the cans. Cooking alarms were broken, water valves leaked and temperature devices were inaccurate, all blamed on poor management. All eight victims were hospitalized and placed on ventilators. It was the first botulism in commercial canned food in the United States in over 30 years.

  In June 1989, the United Kingdom recorded its largest foodborne botulism outbreak. Of 27 patients, one died, and 25 had eaten one brand of hazelnut yogurt in the week before symptoms began. The producer stopped all yogurt production and withdrew its yogurts from sale. Cans of the hazelnut conserve were recalled, and the public was told to avoid all hazelnut yogurts.

  In July 2002, fourteen Alaskans ate muktuk from a beached whale, and eight developed botulism. Two needed ventilators. Between 1990 and 2000, the CDC recorded 263 foodborne cases from 160 events in the United States, with a case fatality rate of 4 percent. Thirty-nine percent, 103 cases in 58 events, were in Alaska, all tied to traditional Alaska Native foods. In the lower 49 states, home-canned food was implicated in 70 events, about 69 percent.

  From 1985 to 2005, Canada saw 91 confirmed cases of foodborne botulism. Eighty-five percent were in Inuit communities, especially Nunavik, along with First Nations on the coast of British Columbia. The cause was traditionally prepared marine mammal and fish products.

  In April 2015, a church potluck in Lancaster, Ohio led to one death, 21 confirmed cases and 10 suspected ones. The suspected source was a salad of home-canned potatoes. In May 2017, ten people in Sacramento County, California ate nacho cheese dip served at a gas station, and one man died. In 2016, prisoners in a Mississippi prison illegally brewed alcohol from food scraps, known as pruno, and 31 people developed botulism. Researchers found that mild cases shared symptoms with severe ones, though the course and outcomes differed. In 2025-13 cases of infant botulism across 10 states were linked to ByHeart Whole Nutrition Infant Formula, and broad recalls followed.

  In 2021, US health departments reported 273 confirmed and probable cases. Infant botulism made up 66 percent, wound botulism 24 percent and foodborne botulism 8 percent. The remaining 2 percent had other or unknown causes. California accounted for 45 infant cases, or 25 percent, and Pennsylvania for 21, or 12 percent. Wound botulism keeps rising while foodborne and infant cases hold relatively steady.

  From 1958 to 1983, China recorded 986 outbreaks involving 4,377 people and 548 deaths. After the Chinese Communist Revolution in 1949, a mysterious plague named Qapqal disease struck several Sibe villages in Qapqal Xibe Autonomous County. It followed distinctive epidemic patterns, yet its cause stayed unknown for a long time. It caused deaths and forced some people to leave. In 1958 the Ministry of Health sent a team of experts, who found mainly type A botulism with a few cases of type B. The source was local fermented grain and beans, plus a raw meat food called mi song hu hu. Residents improved their fermentation techniques, and the disease disappeared.

  In 2017, Ukraine had 70 cases with 8 deaths, after 115 cases and 12 deaths the year before. Most came from dried fish, a common local drinking snack. In 2020, Vietnam reported several cases tied to a contaminated vegetarian pâté, and some patients were put on life support.

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• 7. Birds, Cattle, and Horses

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  An estimated 10,000 to 100,000 waterfowl die of botulism every year, and in large outbreaks a million or more birds may die. The disease is commonly called limberneck. Ducks seem to be affected most often, and in the Western United States and Canada an enzootic form is known as western duck sickness. In the wild, warmth, decomposing vegetation and invertebrates can create ideal conditions for toxin to form where birds feed.

  The disease has been reported in rats, mice, chickens, frogs, toads, goldfish, aplysia, squid, crayfish, drosophila and leeches. In commercially raised chickens, mortality ranges from a few birds to 40 percent of the flock.

  In some parts of the world, cattle epidemics show up to 65 percent mortality. Signs include drooling, restlessness, incoordination, urine retention and trouble swallowing. Cattle that lie on their sides are usually close to death. In southern Africa, phosphorus-deficient cattle tend to chew bones and carrion containing clostridial toxins. They develop lame sickness, called lamsiekte.

  Horses show similar signs. Paralysis usually begins in the hindquarters and moves to the front limbs, neck and head. Death generally comes 24 to 72 hours after the first symptoms, from respiratory paralysis. Some foals are found dead with no other signs. Type C toxin has been blamed for grass sickness, a horse condition of rainy, hot summers in Northern Europe, whose main symptom is paralysis of the pharynx.

  Dogs can fall ill after eating bird carcasses or other infected meat, though they resist the more severe effects of type C. Pigs are relatively resistant. Dairy cows raise a different worry. Lactating cows injected with type C toxin showed none in their milk, yet the protocol for fatal cases is still to burn carcasses and withhold potentially contaminated milk.

  Prevention on farms starts with inspecting feed, buying good feed and storing it properly. Poultry litter and carcasses let spores germinate, so they should not be spread on fields that grow feed. Water sources should be checked for dead animals, and fields should be checked for remains before mowing for hay or silage.

  Vaccines for livestock usually need multiple doses 2 to 6 weeks apart, then yearly boosters. Types C and D toxoid is used on cattle in South Africa and Australia. Toxoid also protects mink and pheasants. In Kentucky, where the disease is endemic, vaccination with type B toxoid appears effective.

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• 8. Weapons Programs

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  At Fort Detrick, CIA research on biological warfare ranked anthrax and botulism as the two most effective options. During the 1950s, the biological warfare program found a highly lethal strain. The CIA still held 5 grams of Clostridium botulinum after Nixon's ban on biological warfare in 1969.

  During the Gulf War, American concern shifted to prevention against a possible attack. A weakness appeared. Until the 1990s, the only way to make antitoxin in the United States was to draw antibodies from a single horse named First Flight, which worried Pentagon health officials.

  In May 1986, the American Type Culture Collection sold 5 variants of botulinum to the University of Baghdad. Iraq held many types of germs, including botulism. Reports from the CIA in 1991 show that Iraqis filled shells, warheads and bombs with biological agents such as botulinum, though none were deployed. The Iraqi air force used the code name "tea" for botulinum, and the toxin was also called bioweapon "A."

  From 1990 to 1995, a Japanese cult called Aum Shinrikyo ran laboratories that produced botulinum, anthrax and Q fever agents. The group staged numerous unsuccessful bioterrorism attacks on civilians. It sprayed botulinum toxin from a truck in downtown Tokyo and at Narita airport. No cases of botulism were reported, a reminder that making a toxin and delivering it are separate problems.

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