After tanking up on “pruno,” a bootleg prison wine, eight maximum-security inmates at the Utah State prison in Salt Lake County tried to shake off more than just the average hangover. Their buzz faded into double vision, weakness, trouble swallowing, and vomiting. Tests confirmed that the detainees came down with botulism from their cellblock science experiment. In secret, a prison moonshiner mixed grapefruit, oranges, powdered drink mix, canned fruit, and water in a plastic bag. For the pièce de résistance, he added a baked potato filched from a meal tray weeks earlier and peeled with his fingernails. After days of fermentation and anticipation, the brewer filtered the mash through a sock, and then doled out the hooch to his fellow yardbirds.
The party was short-lived. The potato was a big mistake.
Investigators traced botulism spores to the humble spud. Within hours of the first swig, botulinum toxin infiltrated the prisoners’ nerve cells, causing weakness and paralysis. Three of the men required a breathing tube and ventilator to prevent suffocation. All eight victims received an experimental antitoxin from the Centers for Disease Control and Prevention, and thanks to meticulous supportive care, none died. But recovery from botulism takes weeks to months; the body must regrow new nerve endings to replace the poisoned ones. All told, the hospital bill topped their bar tab—more than $500,000 in fees alone, not including added expenses for transportation, security, and public health investigation.
Botulinum toxin, a protein produced by the bacterium Clostridium botulinum, could be “the most poisonous poison” there is, as writer Carl Lamanna called it in an article for Science, in 1959. First weaponized by Imperial Japan in the 1930s, and later, Nazi Germany, the United States, the Soviet Union, Syria, Iran, Iraq, and North Korea, a single gram of toxin could theoretically kill more than a million people if dispersed into the air and inhaled. But before botulinum toxin became a bioweapon and a smoother of crow's feet as the drug Botox, botulism was historically a foodborne malady, and the toxin lurked in sausage and cured meats.
Botulism, the illness caused by toxin exposure, first received scientific attention in rural Germany in the late 18th century. Officials in Stuttgart saw an increase in “sausage poisoning” in the wake of the Napoleonic wars, possibly due to poor sanitation and widespread poverty. In the 1820s, a young German physician named Justinus Kerner was the first scientist to publish an accurate and comprehensive description of the disease. He analyzed more than 200 cases of suspected sausage poisoning. He fed extracts of these “sour” sausages to animals and described the classic symptoms of botulism. Muscle weakness leading to drooped eye lids, difficulty swallowing, and respiratory failure; altered autonomic nerve function leading to vomiting, pupil dilation, and dry mouth. Brazenly, he sampled a few drops of this extract himself—he survived, though it caused a “great drying out of the palate and pharynx,” a harbinger of Botox’s modern application in treating uncontrollable salivation for those with amyotrophic lateral sclerosis, or Lou Gehrig’s disease. Grateful citizens dubbed the scientist “Wurst-Kerner,” for his pioneering contributions to public health and sausagery. In 1870, another German physician renamed the illness “botulism” after the Latin word “botulus,” or sausage.
For centuries, people dried, smoked, fermented, canned, and neglected their food, naïve to the microbial threat festering within. This changed in the late 19th and early 20th centuries as science moved from the laboratory into the kitchen. In 1895, Émile van Ermengem isolated a spore-forming bacterium from the remnants of a salted ham that killed three musicians in a Belgian outbreak. He confirmed that Kerner’s mysterious sausage—or ham—poison was made by a microbe. Under very specific growth conditions, the active form of the bacterium could be coaxed to grow and produce toxin; under other conditions, the bacterium would retreat into a dormant, or spore form that does not do so.
Early 20th century researchers found Clostridium botulinum spores nearly anywhere: in soil, rivers, lakes, oceans, on vegetable surfaces, and in fish and animal intestines. Laboratory tests demonstrated that spores are durable: they withstand even boiling. When introduced into an optimal, low-oxygen environment—like the inside of a jar or can of food—spores germinate and make the toxin. Given the ubiquity of botulinum spores in the environment, it is surprising that outbreaks were not more frequent.
As food science matured into its own discipline, botulism outbreaks resulting from commercially canned foods dwindled. Food producers could stop toxin production by manipulating temperature, acidity, salt content, moisture, oxygen concentration, and food preservatives such as nitrates or nitrites. Pressure-cooking freshly canned goods at 250 degrees Fahrenheit destroys spores in 20 minutes, enabling safe long-term storage.
Modern foodborne outbreaks occur when botulism control methods are deliberately, or inadvertently, ignored. Homemade foods are now the leading cause of the disease in the U.S., which is not surprising, as only 59 percent of home canners preserving botulism-friendly low acid vegetables actually use a pressure sterilizing process, according to a National Center for Home Food Preservation survey. Fortunately, botulism remains rare nationwide: between 1990 and 2000, 160 outbreaks afflicted only 263 people. And advances in medical care, including antitoxin availability and intensive care units, have decreased the fatality rate from 60 percent in the first half of the 20th century to about 5 percent now.