Effect of Sodium Chloride on Uptake of Substrate by Staphylococcus aureus 196E.

Sodium chloride inhibited a number of biochemical parameters in Staphylococcus aureus 196E. Induction of phospho-ß-galactosidase, synthesis of staphylococcal enterotoxin A, enzyme activity (phospho-ß-galactosidase) and glucose utilization were approximately four times more sensitive to the inhibitory effects of salt than was growth. Uptake of 14C-2-deoxyglucose and respiratory activity with a number of substrates were inhibited also. The breakdown of o-nitrophenyl-ß-galactoside (ONPG) by lactose-grown S. aureus 196E was inhibited by NaCl as well as by other solutes (salts, carbohydrates, amino acids) which suggested that the inhibitory effect is a general one of solutes and not restricted to NaCl. Various ionophores (gramicidin, valinomycin, monensin, lasalocid, m-chlorophenylhydrazone), the H+-ATPase inhibitor (N,N',-dicyclohexylcarbodiimide), and ion channel blockers (quinine, quinidine, chlorpromazinc, tetracaine, verapamil) reversed the inhibitory action of salt on ONPG breakdown by lactose-grown cells; however, these compounds did not reverse NaCl inhibition of glucose utilization. The effects observed here suggest that NaCl (and probably other solutes) exerts an inhibitory effect on transport of substrates into the cells of S. aureus 196E.

Enterotoxin A synthesis in Staphylococcus aureus: inhibition by glycerol and maltose.

Studies indicated that prior growth of Staphylococcus aureus 196E on glycerol or maltose led to cells with repressed ability to produce staphylococcal enterotoxin A (SEA). A PTS- mutant (196E-MA) lacking the phosphoenolpyruvate phosphotransferase system (PTS), derived from strain 196E, showed considerably less repression of SEA synthesis when cells were grown in glycerol or maltose. Since SEA synthesis is not repressed in the PTS- mutant, repression of toxin synthesis by glycerol, maltose or glucose in S. aureus 196E appears to be related to the presence of a functional PTS irrespective of whether the carbohydrate requires the PTS for cell entry. With lactose as an inducer, glucose, glycerol, maltose or 2-deoxyglucose repressed the synthesis of beta-galactosidase in S. aureus 196E. It is postulated that these compounds repress enzyme synthesis by an inducer exclusion mechanism involving phosphorylated sugar intermediates. However, inducer exclusion probably does not explain the mechanism of repression of SEA synthesis by carbohydrates.

Enterotoxin A production in Staphylococcus aureus: inhibition by glucose.

In this study, we investigated the relationship between carbohydrate metabolism and repression of staphylococcus enterotoxin A (SEA) in Staphylococcus aureus 196E and a pleiotrophic mutant derived from strain 196E. The mutant, designated at strain 196E-MA, lacked a functional phosphoenolpyruvate phosphotransferase system (PTS). The mutant produced acid, under aerobic conditions, from only glucose and glycerol. The parent strain contained an active PTS, and aerobically produced acid from a large number of carbohydrates. Prior growth in glucose led to repression of SEA synthesis in the parent strain; addition to the casamino acids enterotoxin production medium (CAS) led to more severe repression of toxin synthesis. The repression was not related to pH decreases produced by glucose metabolism. When S. aureus 196E was grown in the absence of glucose, there was inhibition of toxin production as glucose level was increased in CAS. The inhibition was related to pH decrease and was unlike the repression observed with glucose-grown strain 196E. The inhibition of SEA synthesis in mutant strain 196E-MA was approximately the same in cells grown with or without glucose and was pH related. Repression of SEA synthesis similar to that seen with glucose-grown S. aureus 196E could not be demonstrated in the mutant. In addition, glucose-grown S. aureus 196E neither synthesized beta-galactosidase nor showed respiratory activity with certain tricarboxylic acid (TCA) cycle compounds. Glucose-grown strain 196E-MA, however, did not show suppressed respiration of TCA cycle compounds; beta-galactosidase was not synthesized because the mutant lacked a functional PTS.(ABSTRACT TRUNCATED AT 250 WORDS)