Roles of arginine in growth of Clostridium botulinum Okra B

Abstract

Group I strains of Clostridium botulinum are known to degrade arginine by the arginine deiminase pathway. We have found that C. botulinum Okra B consumed a level of arginine (20 g/liter) higher than the basal requirement for growth (3 g/liter). Arginine was probably the preferred source of nitrogen for biosynthesis but did not serve as a major source of energy. Citrulline and proline were produced as major fermentation products in media containing high levels of arginine, but in media with basal amounts of arginine these products were produced in lower quantities during growth and were later reassimilated. The results indicate that C. botulinum Okra B changes its metabolism during consumption of surplus arginine, and this change is associated with toxin repression, formation of citrulline and proline as end products, and possibly resistance to environmental stresses such as increased acidity and osmolarity.

In vivocommensal control ofClostridioides difficilevirulence

“…These effects cooccurred with CSAR's up-regulation of an arginine deiminase (ADI) fermentation pathway by 20h of C. difficile infection ( Fig. S3B), including the acrD arginine:ornithine antiporter which exports the ornithine product of arginine fermentation, identifiying a cause for the significantly elevated ornithine in CSAR-monocolonized mice (38). In constrast, CBI's ADI pathway was down-regulated at 20h of co-colonization with C. difficile, followed by up-regulation by 24h with expression of its ornithine cyclodeaminase (OCD) which converts ornithine to proline, potentially conserving a proline-convertible carbon source for its Stickland metabolism (Figs.…”

Posttranslational Regulation of Botulinum Neurotoxin Production in Clostridium botulinum Hall A- hyper

“…The genome sequence of C. botulinum strain Hall A- hyper ( 45 ) was examined for the presence of homologs to genes that are known to be involved in arginine catabolism pathways in other organisms including several clostridia ( 37 , 41 – 44 ). The annotated genome of C. botulinum strain Hall A- hyper includes several arc genes central to the arginine deaminase pathway ( 37 , 41 – 43 ), as well as an ornithine catabolism gene (ornithine cyclodeaminase, CLC2447), and two genes ( argG , CLC2544, and argH , CLC2543) controlling arginine formation from citrulline. Catabolism of arginine through the ADI pathway results in the production of ammonia, citrulline, ornithine, carbamoyl phosphate, CO 2 , and ATP, in addition to other metabolites produced from these products ( 35 , 37 , 41 – 43 ).…”

“…In this study, the mechanism underlying the strong suppression of toxin formation by arginine in proteolytic C. botulinum strain Hall A- hyper was investigated. Arginine is an important nutrient for group I C. botulinum strains, which catabolize arginine via an arginine deiminase (ADI) pathway resulting in the formation of metabolites including citrulline, ornithine, carbamoyl phosphate, ATP, and ammonia ( 37 , 38 , 41 ). Arginine deiminase pathways, consisting of a cluster of genes termed arc genes, have also been demonstrated in numerous other organisms, including clostridial species ( 37 , 41 – 44 ).…”

“…Arginine is an important nutrient for group I C. botulinum strains, which catabolize arginine via an arginine deiminase (ADI) pathway resulting in the formation of metabolites including citrulline, ornithine, carbamoyl phosphate, ATP, and ammonia ( 37 , 38 , 41 ). Arginine deiminase pathways, consisting of a cluster of genes termed arc genes, have also been demonstrated in numerous other organisms, including clostridial species ( 37 , 41 – 44 ). In this study, homologous genes comprising an arginine catabolism pathway were identified in the genome of C. botulinum strain Hall A- hyper .…”

Botulinum Neurotoxin Detection Methods for Public Health Response and Surveillance

“…Favorable physiological conditions (pH, redox potential, ionic strength, temperature, water activity, etc) are needed to stimulate the growth of clostridia and toxin production on food substrates (Peck, 2006 ; Anderson et al, 2011 ). Specifically, nitrogenous sources were known to influence clostridial growth, as well as the production of BoNTs (Patterson-Curtis and Johnson, 1989 , 1992 ); high levels of arginine seem to significantly repress toxin production, slow down autolysis and reduce endospore production (Fredrick et al, 2017 ), highlighting the significance of physiological stimuli in toxin formation. Existing commercial food manufacturing practices, processing methods, preservative methods, and agricultural practices can potentially destroy toxin activity.…”