Clostridium botulinum is a strictly anaerobic, spore-forming,gram-positive rod that elaborates a potent exotoxin. The spores are capable of tolerating temperatures of 100°C for hours, whereas moist heat at 120°C usually destroys them. Eight sepa-rate toxin types (A, B, C (alpha), C (beta), D, E, F, and G) have been described. All are neurotoxins with identical mechanism of action; spores are dormant and highly resistant to damage. Toxin types A, B, E, and rarely F cause human disease; type G has been associated with sudden death in several patients in Switzerland. Illness in animals is often caused by types C and D. Toxin C2 has been described as a cytotoxin agent which can cause vascular permeability and death.
■■ Foodborne botulism usually results from consumption of contaminated preserved food—canned meat and meat products, fruits, vegetables, pickles, and fish. A bulging can with peculiar tasting contents should raise the suspicion of botulism. On opening the can, the explosion of air that occurs is usually because of fluid under pressure (overfilled can), rather than gas. Even if gas is present, it may be due to a chemical reaction subsequent to detinning of the can lining. There may be a putrefied smell or taste if food is contaminated with type A or B toxin, but may taste and appear normal if contaminated by type E toxin.
■■ Wound botulism results from wound infection with Cl. botulinum.
■■Infant botulism most probably is caused by contaminated honey. The US Centers for Disease Control stipulate that infants under the age of 6 months not be given honey, and the Honey Industry Council has extended that limit to one year. Although honey has been defined as one source of spores, all cases cannot be attributed to this. In one case, foodborne botulism occurred in an infant following exposure to improperly prepared home-canned baby food contaminated with Botulinum toxin A.
Clostridium botulinum elaborates a powerful exotoxin which is produced intracellularly and is released only on the death and autolysis of the organism. It is probably the most powerful toxin known to man. The lethal dose for human beings is just 1 to 2 mcg or 1 pg/kg. It is a neurotoxin, and despite its potency, acts slowly taking several hours to kill. Based on animal data, the lethal dose in a 70 kg human would be approximately 0.09 to 0.15 mcg IV or IM. The estimated lethal inhalation dose in a 70 kg human is said to be 0.70 to 0.90 mcg.
Germination of spores in food is enhanced under the following conditions: a pH of greater than 4.5, sodium chlo- ride concentration less than 3.5%, or a low nitrite level. Food suspected to be contaminated with botulinum toxin can be rendered completely safe by pressure cooking or boiling for 20 minutes. However spores can withstand boiling at 100° C, even if it is carried out for several hours.
The botulinum toxin is a protein consisting of a single polypep- tide chain with a MW of 900,000 D, which includes the non- toxic protein haemagglutinin and the 150,000 MW neurotoxic component. To become fully active, the single chain molecule must be cleaved by proteolysis to geneate a heavy chain (MW 100,000) that is linked by a disulfide bond to a light chain (MW 50,000). It is the dichain form of the molecule that is responsible for the toxicity of the toxin.
The botulinum toxin enters the preganglionic nerve terminal by endocytosis and binds rapidly (and irreversibly) to the cell membrane. Once inside the cell, it inhibits calcium-dependant exocytosis, thereby preventing release of acetylcholine and resulting in presynaptic blockade. The toxin acts as a zinc- dependant endoprotease to cleave polypeptides that are essen- tial for exocytosis. This diminution of presynaptic function interferes with cholinergic transmission at all acetylcholine- dependant synapses in the peripheral nervous system. There is no effect on the CNS, or on axonal conduction.
Three steps are necessary for toxin-induced neuromuscular blockade: transport across the intestinal wall into the serum; binding to neuronal receptors; and internalisation of bound toxin, an irreversible step leading to impairment of neurotrans- mitter release and resultant neuromuscular blockade. The result is hypotonia with a descending symmetric flaccid paralysis; the blockade is most prominent at the cranial nerves, autonomic nerves, and neuromuscular junction. Incubation Period About 12 to 36 hours (but can occur as early as 3 hours and as late as 16 days), with a median report of symptoms at 3.2days. Type E toxin has the shortest, and type B toxin the longest incubation period. In general, the earlier the onset of symptoms, the more serious the disease and the more protracted the course.
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