Cl.botulinum

Cl.botulinum

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   MORPHOLOGY  PATHOGENESIS  TOXINS  CLINICAL FINDINGS  LABORATORY TESTS  TREATMENT  PREVENTION & CONTROL
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   Clostridium botulinum, which causes botulism, is worldwide in distribution; it is found in soil and occasionally in animal feces.  Clostridium botulinum is a rod-shaped microorganism.  It is an obligate anaerobe, meaning that oxygen is poisonous to the cells.  However,C. botunlinum tolerates traces of oxygen due to the enzyme called superoxide dismutase (SOD) which is an important antioxidant defense in nearly all cells exposed to oxygen.   C. botulinum does not form endospores as a way to protect the viability of the organism, but rather as a mechanism to produce the neurotoxin.   C. botulinum is only able to produce the neurotoxin during sporulation, which can only happen in an anaerobic environment.
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   Other bacterial species produce spores in an unfavorable growth environment to preserve the organism's viability and permit survival in a dormant state until the spores are exposed to favorable conditions.  In the laboratory Clostridium botulinum is usually isolated in tryptose sulfite cycloserine (TSC) growth media in an anaerobic environment with less than 2% of oxygen.  C. botulinum is a lipase negative microorganism that grows between pH of 4.8 and 7 and it can't use lactose as a primary carbon source  Spores of the organism are highly resistant to heat, withstanding 100 °C for several hours.
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   Although C.botulinum types A and B have been implicated in cases of wound infection and botulism, most often the illness is not an infection.  Rather, it is an intoxication resulting from the ingestion of food in which C botulinum has grown and produced toxin.  The most common offenders are spiced, smoked, vacuum- packed, or canned alkaline foods that are eaten without cooking.  In such foods, spores of C botulinum germinate; under anaerobic conditions, vegetative forms grow and produce toxin.  The toxin acts by blocking release of acetylcholine at synapses and neuromuscular junctions.  Flaccid paralysis results. [reduced muscle tone]  The electromyogram strength tests are typical.
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   During the growth of C botulinum and during autolysis of the bacteria, toxin is liberated into the environment.  Seven antigenic varieties of toxin (A–G) are known.  Types A, B, and E (and occasionally F) are the principal causes of human illness.  Types A and B have been associated with a variety of foods  Type E predominantly with fish products.  Type C produces limberneck in birds;  Type D causes botulism in mammals.  The toxin is a 150,000-MW protein that is cleaved into 100,000-MW and 50,000-MW proteins linked by a disulfide bond.
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   Botulinum toxin is absorbed from the gut and binds to receptors of presynaptic membranes of motor neurons of the peripheral nervous system and cranial nerves.  Proteolysis—by the light chain of botulinum toxin—of the target proteins in the neurons inhibits the release of acetylcholine at the synapse, resulting in lack of muscle contraction and paralysis.  The proteins are synaptobrevin, SNAP 25, and syntaxin.  The toxins of C botulinum types A and E cleave the 25,000- MW SNAP-25.  Type B toxin cleaves synaptobrevin.  C botulinum toxins are among the most toxic substances known: The lethal dose for a human is probably about 1–2 g.  The toxins are destroyed by heating for 20 minutes at 100 °C.
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   Symptoms begin 18–24 hours after ingestion of the toxic food, with visual disturbances (incoordination of eye muscles, double vision), inability to swallow, and speech difficulty;  signs of paralysis are progressive, and death occurs from respiratory paralysis or cardiac arrest.  Gastrointestinal symptoms are not regularly prominent.  There is no fever.  The patient remains fully conscious until shortly before death.  In the United States, infant botulism is as common as or more common than the classic form of paralytic botulism associated with the ingestion of toxin-contaminated food.
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   The infants in the first months of life develop poor feeding, weakness, and signs of paralysis ("floppy baby").  Infant botulism may be one of the causes of sudden infant death syndrome.  C botulinum and botulinum toxin are found in feces but not in serum.  It is assumed that C botulinum spores are in the babies' food, yielding toxin production in the gut.  Honey has been implicated as a possible vehicle for the spores.
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   Mice injected with toxin intraperitoneally die rapidly.  The antigenic type of toxin is identified by neutralization with specific antitoxin in mice.  C botulinum may be grown from food remains and tested for toxin production.  In infant botulism, C botulinum and toxin can be demonstrated in bowel contents but not in serum.  Toxin may be demonstrated by passive hemagglutination or radioimmunoassay.
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   Potent antitoxins to three types of botulinum toxins have been prepared in horses.  Since the type responsible for an individual case is usually not known, trivalent (A, B, E) antitoxin must be promptly administered intravenously with customary precautions.  Adequate ventilation must be maintained by mechanical respirator, if necessary.  These measures have reduced the mortality rate from 65% to below 25%.  Although most infants with botulism recover with supportive care alone, antitoxin therapy is recommended.
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   Botulinum toxin is considered to be a major agent for bioterrorism and biologic warfare.  Since spores of C botulinum are widely distributed in soil, they often contaminate vegetables, fruits, and other materials.  A chief risk factor for botulism lies in home-canned foods, particularly string beans, corn, peppers, olives, peas, and smoked fish or vacuum-packed fresh fish in plastic bags.  Toxic foods may be spoiled and rancid, and cans may "swell," or the appearance may be innocuous.  When such foods are canned or otherwise preserved, they either must be sufficiently heated to ensure destruction of spores or must be boiled for 20 minutes before consumption.