Clostridium Species

Clostridium Species
The clostridia are large anaerobic, gram-positive, motile rods. Many decompose proteins or form toxins, and some do both. Their natural habitat is the soil or the intestinal tract of animals and humans, where they live as saprophytes. Among the pathogens are the organisms causing botulism, tetanus, gas gangrene, and pseudomembranous colitis.
Morphology & Identification
Spores of clostridia are usually wider than the diameter of the rods in which they are formed. In the various species, the spore is placed centrally, subterminally, or terminally. Most species of clostridia are motile and possess peritrichous flagella.
Culture
Clostridia are anaerobes and grow under anaerobic conditions; a few species are aerotolerant and will also grow in ambient air.
Colony Forms
Some clostridia produce large raised colonies (eg, C perfringens); others produce smaller colonies (eg, C tetani). Some clostridia form colonies that spread on the agar surface. Many clostridia produce a zone of hemolysis on blood agar. C perfringens typically produces multiple zones of hemolysis around colonies.
Growth Characteristics
Clostridia can ferment a variety of sugars; many can digest proteins. Milk is turned acid by some and digested by others and undergoes "stormy fermentation" (ie, clot torn by gas) with a third group (eg, C perfringens).
Clostridium botulinum
Clostridium botulinum, which causes botulism, is worldwide in distribution; it is found in soil and occasionally in animal feces.
Types of C botulinum are distinguished by the antigenic type of toxin they produce. Spores of the organism are highly resistant to heat, withstanding 100 °C for several hours. Heat resistance is diminished at acid pH or high salt concentration.
Toxin
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 and type E predominantly with fish products. Type C produces 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. 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. & this toxin cause in the neurons inhibits the release of acetylcholine at the synapse, resulting in lack of muscle contraction and paralysis.
Pathogenesis
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.
Clinical Findings
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 bulbar paralysis are progressive, and death occurs from respiratory paralysis or cardiac arrest. Gastrointestinal symptoms are not regularly prominent. There is no fever.
Diagnostic Laboratory Tests
Toxin can often be demonstrated in serum from the patient, and toxin may be found in leftover food. Mice injected intraperitoneally die rapidly. The antigenic type of toxin is identified by neutralization with specific antitoxin in mice. Also Toxin may be demonstrated by passive hemagglutination or radioimmunoassay.
Treatment
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.