Botulism is a rare, life-threatening paralytic illness caused by neurotoxins produced by an anaerobic, gram-positive, spore-forming bacterium, Clostridium botulinum. Unlike Clostridium perfringens, which requires the ingestion of large numbers of viable cells to cause symptoms, the symptoms of botulism are caused by the ingestion of highly toxic, soluble exotoxins produced by C. botulinum while growing in foods.
These rod-shaped bacteria grow best under anaerobic (or, low oxygen), low-salt, and low-acid conditions. Bacterial growth is inhibited by refrigeration below 4° C., heating above 121° C, and high water-activity or acidity. And although the toxin is destroyed by heating to 85° C. for at least five minutes, the spores formed by the bacteria are not inactivated unless the food is heated under high pressure to 121° C. for at least twenty minutes.
The incidence of foodborne botulism is extremely low. Nonetheless, the extreme danger posed by the bacteria has required that “intensive surveillance is maintained for botulism cases in the United States, and every case is treated as a public health emergency.” This danger includes a mortality rate of up to 65% when victims are not treated immediately and properly. Most of the botulism events that are reported annually in the United States are associated with home-canned foods that have not been safely processed. Very occasionally, however, commercially- processed foods are implicated as the source of a botulism events, including sausages, beef stew, canned vegetables, and seafood products.
After their ingestion, botulinum neurotoxins are absorbed primarily in the duodenum and jejunum, and pass into the bloodstream and travel to synapses in the nervous system. There, the neurotoxins cause flaccid paralysis by preventing the release of acetylcholine, a neurotransmitter, at neuromuscular junctions, thereby preventing motor-fiber stimulation. The flaccid paralysis progresses symmetrically downward, usually starting with the eyes and face, and then moving to the throat, chest, and extremities. When the diaphragm and chest muscles become fully involved, respiration is inhibited and, unless the patient is ventilated, death from asphyxia results. Classic symptoms of botulism include nausea, vomiting, fatigue, dizziness, double vision, drooping eyelids, slurred speech, difficulty swallowing, and dryness of skin, mouth, and throat, lack of fever, muscle weakness, and paralysis. Infants with botulism appear lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone. Throughout all such symptoms, the victims are fully alert and the results of sensory examination are normal.
In foodborne botulism cases, symptoms usually begin anywhere between 12 and 72 hours after the ingestion of toxin-containing food. Longer incubation periods—up to 10 days—are not unknown, however. The duration of the illness is from 1 to 10 (or more) days, depending on host-resistance, the amount of toxin ingested, and other factors. Full recovery often takes from weeks to months. And, as earlier indicated, mortality rate can be from 30% to 65%, with rates generally lower in European countries than in the United States.
Detection and treatment
Although botulism can be diagnosed based on clinical symptoms, its differentiation from other diseases is often difficult—especially in the absence of other known persons affected by the condition. Once suspected, the most direct and effective way to confirm the diagnosis of botulism in the laboratory is testing for the presence of the botulinum toxin in the serum, stool, or gastric secretions of the patient. The food consumed by the patient can also be tested for the presence of toxins. Currently, the most sensitive and widely used method for the detection of the toxins is the mouse neutralization test, which involves injecting serum into mice and looking for signs of botulism. This test typically takes 48 hours, while the direct culturing of specimens takes 5-7 days. Some cases of botulism may go undiagnosed because symptoms are transient or mild, or are misdiagnosed as Guillain-Barre Syndrome.
If diagnosed early, foodborne botulism can be treated with an antitoxin that blocks the action of toxin circulating in the blood. This can prevent patients from worsening, but recovery still takes many weeks. The mainstay of therapy is supportive treatment in intensive care, and mechanical ventilation in case of respiratory failure, which is common.
Long-Term and Permanent Injury
Although a minority of botulism patients eventually recovers their pre-infection health, the majority does not. For those who fully recover, the greatest improvement in muscle strength occurs in the first three months after the acute phase of illness. The outside limit for such improvement appears, however, to be one year. Consequently, physical limitations that still exist beyond the one-year mark are more probably than not permanent. Recovery from acute botulism symptoms may also be followed by persistent psychological dysfunction that may require intervention.
According to a recently published study that tracked the long-term outcomes of 217 cases of botulism, a large majority of patients reported “significant health, functional, and psychosocial limitations that are likely the consequences of the illness.” These limitations included: fatigue, weakness, dizziness, dry mouth, and difficulty lifting things. The victims also reported difficulty breathing caused by moderate exertions, such as walking or lifting heavy items. They were also more likely to have limitations in vigorous activities, like running or playing sports, climbing up three flights of stairs, or carrying groceries. Summarizing its finding, the study concluded that:
Even several years after acute illness, patients who had botulism were more likely than control subjects to experience fatigue, generalized weakness, dizziness, dry mouth, difficulty lifting things, and difficulty breathing caused by moderate exertion. In addition, patients reported worse overall psycho-social status than did control subjects, with patients being significantly less likely to report feeling happy, calm and peaceful, or full of pep.
There is, as a result, no question that the damaging effects of botulism are life-long.
Some background information on canning
The canning process dates back to the late 18th century in France when the Emperor Napoleon Bonaparte, concerned about keeping his armies fed, offered a cash prize to whoever could develop a reliable method of food preservation. Nicholas Appert conceived the idea of preserving food in bottles, like wine. After fifteen years of experimentation, he realized if food is sufficiently heated and sealed in an airtight container, it would not spoil. More than fifty years later, Louis Pasteur provided the explanation for effectiveness of canning when he was able to demonstrate that the growth of microorganisms is the cause of food spoilage.
An Englishman, Peter Durand, took the idea one step further and replaced the breakable glass bottles with cylindrical tinplate canisters (later shortened to “cans”). Durand did not can foods himself, but sold his patent to two other Englishmen, Bryan Donkin and John Hall, who set up a commercial canning factory. By 1813, Donkin and Hall were busily producing their first canned goods for the British army, thus continuing the connection of canning to the military.
The basic principles of canning have not changed dramatically since Nicholas Appert and Peter Durand developed the process. Heat sufficient to destroy microorganisms is applied to foods packed into sealed, or “airtight” containers. The canned foods are then heated under steam pressure at temperatures of 240-250°F (116-121°C). The amount of time needed for processing is different for each food, depending on the food’s acidity, density and ability to transfer heat.
Processing conditions are chosen and designed to be the minimum needed to ensure that the foods are made “commercially sterile,” while still retaining the greatest flavor and nutrition. The U.S. Food and Drug Administration must first approve all canning-processes. Once the cans are sealed and heat processed, the resulting canned food must maintain its high eating quality for more than two years and be safe to eat as long as the can is not damaged in any way. Historically, commercially canned food has a near-perfect track record, having caused only four outbreaks in over forty years. The last outbreak occurred in 1974 and involving beef stew.
Bill Marler is an accomplished personal injury and products liability attorney. He began litigating foodborne illness cases in 1993, when he represented Brianne Kiner, the most seriously injured survivor of the Jack in the Box E. coli O157:H7 outbreak. Bill settled Brianne’s case for $15.6 million, creating a Washington state record for an individual personal injury action.
Bleck, supra note 15, at 2547. See also P. Wilcox, et al., Recovery of Ventilatory and Upper Airway Muscles and Exercise Performance After Type-A Botulism, Chest, 98:620-26 (1990); J. Mann, et al., Patient Recovery From Type-A Botulism: Morbidity Assessment Following a Large Outbreak, Am. J. Public Health, 71 (3): 266-69 (Mar. 1981).
Bleck, supra note 15, at 2547. See also F. Cohen, et al., Physical and Psychosocial Health Status 3 Years After Catastrophic Illness—Botulism, Issues Mental Health Nurs., 9:387098 (1988).
S. Gottlieb, et al., Long-Term Outcomes of 217 Botulism Cases in the Republic of Georgia, Clin. Infectious Disease, 45: 174-80, at 180 (220).
St Louis ME, Peck SH, Bowering D, et al. Botulism from chopped garlic: delayed recognition of a major outbreak. Ann Intern Med 1998;108:363.
Morse DL, Pickard LK, Guzewich JJ, et al. Garlic-in-oil associated botulism: episode leads to product modification. Am J Public Health 1990; 80:1372.
See J. Sobel, et al., Foodborne Botulism in the United States, 1990-2000, Emerging Infectious Diseases, Vol. 10, No. 9, at 1606 (Sept. 2004).
James M. Jay, MODERN FOOD MICROBIOLOGY, 466 (6th Ed. 2000).
Id. at 469-71; see also Sobel, supra note 2, at 1606.
Jay, supra note 3, at 467-69. See also, generally H. Houschild, Clostridium Botulinum, in FOODBORNE BACTERIAL PATHOGENS, at 112-89 (M. Doyle Ed. 1989). With botulism, the broader term “event” is used to encompass both outbreaks—i.e., two or more cases of botulism caused by a common-source, as well as individual (or sporadic) cases.
Thomas P. Bleck, Clostridium botulinum (Botulism), in MANDELL, DOUGLAS AND BENNETT’S PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASE 2543, 2544 (5th ed. 2000). see also BOTULISM FACT SHEET, National Agricultural Bio-Security Center, Kansas State University, online at http://nabc.ksu.edu/content/factsheets/category/Botulism#f26.
R. Shapiro, et al., Botulism in the United States: A Clinical and Epidemiologic Review, Ann. Intern. Med. 1998; 129:221-28.
FDA/CFSAN Bad Bug Book, Clostridium Botulinum, available at http://vm.cfsan.fda.gov/~mow/chap2.html
The following introductory material is based on information from the Wikipedia entry on canning, online at http://en.wikipedia.org/wiki/Canning, and the sources there cited.
Tony Baird-Packer, The Production of Microbiologically Safe and Stable Foods, in Volume 1 of THE MICROBIOLOGICAL SAFETY AND QUALITY OF FOOD, 4 (B. Lund, et al. Eds. 2000).
See, e.g. MMWWR, supra note 1, at 3 (citing P. Blake, et al., Type A Botulism from Commercially-Canned Beef Stew, South. Med. J. 1977; 70:5-7).
The information about the outbreak comes primarily from the CDC-published report issued July 30, 2007. See MMWR, supra note 1, at 1-2.