A strain of Salmonella typhimurium in which the genes encoding the general phosphoenolpyruvate :sugar phosphotransferase system (PTS) proteins HPr and Enzyme I have been deleted, the normally cryptic gene encoding the fructoseinducible Enzyme I (EI* or EI fructose ) is expressed, and the fructose repressor protein is inactive (fruR or cra mutant) was studied. This strain lacks HPr and EI, but expresses FPr (DTP) and EI fructose constitutively. Since FPr and EI fructose can substitute for HPr and EI, the strain grew in minimal liquid medium supplemented with the PTS sugars glucose, fructose, N-acetylglucosamine, mannitol or mannose. However, it showed very poor to negligible growth on the PTS sugar glucitol. It also grew very poorly on the non-PTS sugars maltose, melibiose and especially glycerol. Adding cAMP to the medium allowed growth on glucitol, but did not affect growth on glycerol. We suggest that poor phosphorylation of the regulatory molecule Enzyme IIA glucose by FPr is responsible for these effects.
have disclosed no relevant financial relationships. Susan Madison-Antenucci, PhD, has disclosed the following relevant financial relationships: received grants for clinical research from Grifols.
In early June, the New York City syndromic surveillance system detected five signals in sales of over-the-counter antidiarrheal medications. To determine if this increase reflected a concerning cluster of diarrheal illness, we examined multiple communicable disease surveillance data systems. After further investigation of syndromic and other systems, we determined that findings possibly reflected sales promotions but did not suggest increased diarrheal illness in NYC.
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