Clostridial spores

Infectious botuhsm is a consequence of ingesting or inhaling clostridial spores which colonize the large intestines. 

Infant botulism is a consequence of intoxication by BoNT following ingestion or inhalation of clostridial spores that colonize the large intestine young infants. 

In contrast, the benefit of using nitrites in certain foods is not in doubt. Nitrites have the remarkable property of inhibiting the germination of clostridial spores such as those of the deadly CL botulinum. Without the use of nitrite, products such as salt beef, pressed meat loaves , luncheon meats, the larger sizes of canned ham... 

Tetanus is a disease caused by the release of neurotoxins from the anaerobic, spore-forming rod Clostridium tetani. The clostridial protein, tetanus toxin, possesses a protease activity which selectively degrades the pre-synaptic vesicle protein synaptobrevin, resulting in a block of glycine and y-aminobutyric acid (GABA) release from presynaptic terminals. Consistent with the loss of neurogenic motor inhibition, symptoms of tetanus include muscular rigidity and hyperreflexia. The clinical course is characterized by increased muscle tone and spasms, which first affect the masseter muscle and the muscles of the throat, neck and shoulders. Death occurs by respiratory failure or heart failure. 

Lee et al. (1978) investigated the possibility that sulfhydryl groups were required in the formation of the clostridial inhibitor in cured meats. Sulfhydryl groups of meat proteins were blocked by treatment with silver lactate, then the samples were cooked with sodium nitrite before inoculation with C. botuli num spores. Botulinal growth as measured by gas and toxin production was similar to controls without silver lactate treatment. They thus concluded that sulfhydryl groups were not required for the antibotulinal effects of nitrite in cured meats. 

Gastrointestinal colonization in adults or children by clostridial bacteria does not typically take place except under circumstances where the normal flora has been altered by antibiotic treatment (Cheiington, 1998). Botulism results from in vivo production of toxin, analogous to the pathogenesis of infant botulism (McCroskey and Hatheway, 1988 Chia et al, 1986). Support for this form of botulism is provided by demonstration of prolonged excretion of toxin and C. botulinum in stool and/or by the demonstration of C. botulinum spores but not preformed toxin in suspected foods. 

Tracy BP, Jones SW, Papoutsakis ET. (2011). Inactivation of 6 and 6° in Clostridium acetobutylicum illuminates their roles in clostridial-cell-form biogenesis, granulose synthesis, solventogenesis, and spore morphogenesis. J Bacterial, 193,1414—1426. 

The most important property of the genus Propionibacterium is the production of propionic acid as a result of the propionic acid fermentation dependent on coenzyme B12. If the dependence on coenzyme Bn is disregarded, some clostridial strains that do not form spores may be erroneously attributed as propionibacteria. For example, Cl botulinum, Cl propionicum and some other species can produce propionic acid, but propionibacteria have the GC-type DNA (65-67 mol% G+C in classical and 53-62 mol% in cutaneous bacteria), while clostridial DNA is of the AT-type (25-30 mol% G+C). 

Infant botulism has been observed in babies of 3-35 weeks where ingestion of C. botulinum spores leads to the organisms growth and production of the neurotoxin in the intestine (Miduara and Amon, 1976 Pickett et al., 1976). Recently, non-botulinum clostridial species, such as Clostridium butyricum and C. barati have been found to be responsible for human botulism cases (McCrosckey et al., 1988 Amon, 1992). In addition, botulism has been held responsible for several sudden infant death syndrome (SIDS) cases (Amon, 1992). 

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