Clostridium botulinum

Overview: Clostridium botulinum is a large, Gram-positive, spore-forming, rod-shaped anaerobic bacterium, widely distributed in soil, sediments of lakes and ponds, and decaying vegetation (Figure 1). This pathogen produces botulinum toxin, a very potent toxin similar in structure to tetanus toxin, which causes botulism. C. Botulinum can be found on many types of food, specifically foods with a pH above 4.6. Most food processing techniques destroy C. Botulinum spores; however, improper preparation or processing can result in bacterial contamination.

Figure 1. A photomicrograph of Clostridium botulinum stained with Gentian violet.

Currently, there are seven known types of C. botulinum classified by the antigenic specificity of the toxin they produce. Types A (Figure 2), B, E and F are responsible for human cases of botulism, while types C and D cause most cases of botulism in animals. In humans, there are four types of botulism caused by C. Botulinum: Foodborne, wound, infant, and another with a yet to be determined classification. All forms of botulism have a high mortality rate if not treated immediately.

Figure 2. A photomicrograph of Clostridium botulinum type A viewed using a Gram stain technique. The bacterium C. botulinum produces a nerve toxin, which causes the rare, but serious paralytic illness botulism.

Virulence and Pathogenicity: Generally, botulinum toxin is one of the most potent toxins known (Pier et al., 2004) (Figure 3). The most common cause of botulism is from contaminated food, where spores of this organism germinate in sealed food containers under anaerobic conditions and elaborate the toxin. Food-borne botulism is very serious, not only for the rapidity with which the toxin works and its potential to paralyze muscles needed for breathing, but also because additional cases can occur from individuals who eat similarly contaminated foods. When contaminated food is ingested, the toxin is absorbed in the upper gastrointestingal tract, and passes to the blood stream where it reaches the peripheral neuromuscular synapse. There the toxin binds to presynaptic terminals, blocking the release of acetylcholine which is required for muscle stimulation. Symptoms of foodborne botulism begin 18 to 36 hours after ingestion of botulinum toxin containing food. Symptoms include weakness, fatigue and vertigo, followed by neurological failures such as blurred or doubled vision, inability to swallow, difficulty in speech, and descending weakness of skeletal muscles. If left untreated respiratory paralysis can occur.

Figure 3. Protein structure of botulinum toxin.

Furthermore, Infants are susceptible to botulism when spores from contaminated food, such as honey, germinate in their gastrointestinal tract. Wounds can also be infected by C. botulinum whose spores germinate in the wounded tissue and produce toxin. Both foodborne and wound botulism share the same symptoms and risks. Infant botulism occurs 5 to 20 weeks of age, which have been exposed to solid foods, which are presumed to be the source of infection. C. Botulinum establishes itself in the bowels of infants before normal intestinal bacteria, resulting in production of botulinum toxin. Symptoms of infant botulism are constipation, a weak sucking ability, and general weakness. The fourth and yet to be classified type of botulism occurs in adult cases in which a specific food or wound source cannot be identified. It is speculated that this type of botulism may result from intestinal colonization in adults.

Diagnosis and Treatment: Diagnosis of botulism can be made through clinical symptoms alone; however differentiation from other illnesses may be difficult. Therefore direct demonstration of toxin in the blood serum or feces of the patient, or in the food itself is the best method of diagnoses.

Immunity to botulism is clearly mediated by toxin-neutralizing antibodies, a supply of which is kept by the Centers for Disease Control (CDC) for use with small numbers of cases; however, once botulinum toxin has bound to a nerve ending, it is no longer affected by the antitoxin, necessitating early treatment. With proper supportive care, such as mechanical ventilation, people can recover from botulism, but this takes a long time and is expensive. Interestingly, immunity to botulinum toxin never develops naturally, as the amount of toxin required to produce an immune response is lethal, and although a vaccine is possible, it is impractical due to the infrequency of the disease. Curiously, widespread use of a vaccine for botulism may meet resistance as minute does of the toxin, known as Botox, are being used as a treatment for cosmetic disorders. A vaccine could render this therapy ineffective (Pier et al., 2004).

Compare and contrast the pathogenicity of Clostridium botulinum and Clostridium tetani, including mechanisms of action of their toxins and disease manifestations.

Both bacteria are anaerobic endospores-formers that produce neurotoxins. Disease results when the endospores are introduced deep into the tissues. Both neurotoxins interfere with motor control.

Botulism toxin, produced by C. botulinum, binds the cytoplasmic membranes of motor neurons at the synapse and prevents the release of acetylcholine neurotransmitter, and consequently prevents signaling to muscle cells. When muscle cells do not receive signals from motor neurons, they remain relaxed, which result in a flaccid paralysis. A long list of symptoms is produced by the lack of motor control, the most serious of which is respiratory failure, since respiratory muscles can be affected by botulism toxin.

Tetanus toxin, produced by C. tetani, targets inhibitory neurons, which release inhibitory neurotransmitter that prevents muscle cells from responding to acetylcholine stimulation to contract. Under normal circumstances, when one muscle of an antagonistic pair is stimulated to contract, the other muscle is inhibited from contracting, allowing for normal movement by alternate flexion and extension. When tetanus toxin blocks the release of inhibitory neurotransmitter, both muscles of the antagonistic pair contract spasmodically, and sometimes lock in continuous contraction, resulting in non-flaccid paralysis. Loss of control of the respiratory muscles can lead to respiratory failure. Tetanus toxin can also interfere with autonomic (non-voluntary) muscle control, which may result in irregular heartbeat and possibly heart failure.


Pier, G., Lyczak, J., & Wetzler, L. (2004). Immunology, Infection, and Immunity. American Society for Microbiology. Washington, DC.