Clostridium botulinum are rod-shaped bacteria (also called C. botulinum). They are anaerobic, meaning they live and grow in low oxygen conditions. The bacteria form protective spores when conditions for survival are poor. The spore has a hard protective coating that encases the key parts of the bacterium and has layers of protective membranes. Within these membranes and the hard coating, the dormant bacterium is able to survive for years. C. botulinum is responsible for a disease called botulism.
Botulism is a life-threatening disease caused by the ingestion of a potent neurotoxin produced during growth of the C. botulinum bacteria. This neurotoxin is among the most toxic substances known; even microscopic amounts can cause illness or death. In the past, botulism was linked primarily to home-canned foods. In recent decades, however, botulism illnesses have been linked to foods such as unrefrigerated homemade salsa, baked potatoes sealed in aluminum foil, honey (the primary cause of botulism in infants), garlic in oil, and traditionally prepared salted or fermented fish.
There are five main kinds of botulism:
• Foodborne botulism
• Wound botulism
• Infant botulism
• Adult intestinal toxemia (adult intestinal colonization) botulism
• Inadvertent botulism All forms of botulism can be fatal and are considered medical emergencies.
Foodborne botulism is a public health emergency because many people can be poisoned by eating a contaminated food.
Botulism is characterised by symmetrical, descending, flaccid paralysis of motor and autonomic nerves usually beginning with cranial nerves. It occurs when neuromuscular transmission is interrupted by a protein neurotoxin produced by the spore-forming, obligate anaerobic bacterium Clostridiumbotulinum.
Paralysis begins with the cranial nerves, then affects the upper extremities, the respiratory muscles, and, finally, the lower extremities in a proximal-to-distal pattern. In severe cases, extensive respiratory muscle paralysis leads to ventilatory failure and death unless supportive care is provided.
Summary of clinical effects
Onset generally occurs 18 to 36 hours after exposure (range, 6 hours to 8 days). Initial symptoms can include nausea, vomiting, abdominal cramps or diarrhoea. After the onset of neurologic symptoms, constipation is typical. Dry mouth, blurred vision, and diplopia are usually the earliest neurologic symptoms. They are followed by dysphonia, dysarthria, dysphagia, and peripheral muscle weakness. Symmetric descending paralysis is characteristic of botulism.
This can be defined as clinical evidence of botulism following lesions, with a resultant infected wound and no history suggestive of foodborne illness. Except for the gastrointestinal symptoms, the clinical manifestations are similar to those seen in foodborne botulism. However, the incubation period is much longer as time is required for the incubation of spores, growth of clostridium and release of toxins (4 to 14 days).
This is caused by the absorption of toxin produced by Clostridium botulinum that colonize the intestinal tracts of infants under one year of age. It is often associated with ingestion of honey and the first clinical sign is usually constipation. After a few weeks, progressive weakness and poor feeding are observed. The weakness is symmetrical and descending. It evolves over hours or several days.
The infant is afebrile and has a weak cry, has either absent or diminished spontaneous movements, decreased sucking, floppy head and decreased motor response to stimuli. The autonomic nervous system manifestations include dry mucous membranes, urinary retention, diminished gastro-intestinal motility, fluctuation of heart rate, and changes in skin colour. Duration of hospitalisation may last from a few days to six months.
Adult infectious botulism
It occurs as a result of intestinal colonization with C. botulinum and in vivo toxin production in a manner similar to that of infant botulism. These patients often have a history of abdominal surgery, achlorhydria, Crohn’s disease or recent antibiotic treatment. The disease may simulate a Guillain- Barré Syndrome.
This has been reported in patients who have been treated with intramuscular injections of botulinum toxin. Marked clinical weakness is observed as well as electrophysiologic abnormalities.
How is botulism diagnosed?
Physicians may consider the diagnosis if the patient’s history and physical examination suggest botulism. However, these clues are usually not enough to allow a diagnosis of botulism. 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, spinal fluid examination, nerve conduction test (electromyography, or EMG), and a tensilon test for myasthenia gravis. Tests for botulinum toxin and for bacteria that cause botulism can be performed at some state health department laboratories and at CDC.
Are there complications from botulism?
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 perccent to 3-5 percent. A patient with severe botulism may require a breathing machine as well as intensive medical and nursing care for several months, and some patients die from infections or other problems related to remaining paralyzed for weeks or 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 recovery.
What is the Best Way to Prevent Botulism?
The control of foodborne botulism is based almost entirely on thermal destruction (heating) of the spores or inhibiting spore germination into bacteria and allowing cells to grow and produce toxins in foods. To prevent foodborne botulism:
• Use approved heat processes for commercially and home-canned foods (i.e., pressure-can low-acid foods such as corn or green beans, meat, or poultry).
• Discard all swollen, gassy, or spoiled canned foods. Double bag the cans or jars with plastic bags that are tightly closed. Then place the bags in a trash receptacle for non-recyclable trash outside the home. Keep it out of the reach of humans and pets.
• Do not taste or eat foods from containers that are leaking, have bulges or are swollen, look damaged or cracked, or seem abnormal in appearance. Do not use products that spurt liquid or foam when the container is opened.
• Boil home-processed, low-acid canned foods for 10 minutes prior to serving. For higher altitudes, add 1 minute for each 1,000 feet of elevation.
• Refrigerate all leftovers and cooked foods within 2 hours after cooking (1 hour if the temperature is above 90 °F).
• One of the most common causes of foodborne botulism is improperly home-canned food, especially low-acid foods such as vegetables and meats. Only a pressure cooker/canner allows water to reach 240 to 250 °F, a temperature that can kill the spores.
How can botulism be treated?
The respiratory failure and paralysis that occur with severe botulism may require a patient to be on a breathing machine (ventilator) for weeks or months, plus intensive medical and nursing care. The paralysis slowly improves. Botulism can be treated with an antitoxin which blocks the action of toxin circulating in the blood.
Antitoxin for infants is available from the California Department of Public Health, and antitoxin for older children and adults is available through CDC. If given before paralysis is complete, antitoxin can prevent worsening and shorten recovery time.
Physicians may try to remove contaminated food still in the gut by inducing vomiting or by using enemas. Good supportive care in a hospital is the mainstay of therapy for all forms of botulism.