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Inhibition of fructan‐fermenting equine faecal bacteria and S treptococcus bovis by hops ( H umulus lupulus L .) β ‐acid
Author(s) -
Harlow B.E.,
Lawrence L.M.,
Kagan I.A.,
Flythe M.D.
Publication year - 2014
Publication title -
journal of applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 1364-5072
DOI - 10.1111/jam.12532
Subject(s) - streptococcus bovis , fermentation , fructan , biology , inulin , bacteria , microbiology and biotechnology , hindgut , food science , fibrobacter succinogenes , lactic acid , biochemistry , sucrose , botany , rumen , genetics , larva , midgut
Aims The goals of this study were to determine if β ‐acid from hops ( Humulus lupulus L.) could be used to control fructan fermentation by equine hindgut micro‐organisms, and to verify the antimicrobial mode of action on Streptococcus bovis , which has been implicated in fructan fermentation, hindgut acidosis and pasture‐associated laminitis (PAL) in the horse. Methods and Results Suspensions of uncultivated equine faecal micro‐organisms produced fermentation acids when inulin (model fructan) was the substrate, but β ‐acid (i.e. lupulone) concentrations ≥9 ppm inhibited lactate production and mitigated the decrease in pH. Inulin‐fermenting Strep. bovis was isolated from the β ‐acid‐free suspensions after enrichment with inulin. The isolates were sensitive to β ‐acid, which decreased the viable number of streptococci in faecal suspensions, as well as growth, lactate production and the intracellular potassium of Strep. bovis in pure culture. Conclusions These results are consistent with the hypothesis that hops β ‐acid prevented the growth of fructan‐fermenting equine faecal bacteria, and that the mechanism of action was dissipation of the intracellular potassium of Strep. bovis . Significance and Impact of the Study Bacterial hindgut fermentation of grass fructans has been linked to PAL and other metabolic disorders in horses. Hops β ‐acid is a potential phytochemical intervention to decrease the growth of bacteria responsible for PAL.