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ARS Home » Northeast Area » Ithaca, New York » Robert W. Holley Center for Agriculture & Health » Research » Publications at this Location » Publication #111722

Title: THE NISIN RESISTANCE OF STREPTOCOCCUS BOVIS

Author
item MANTOVANI, HILARIO
item Russell, James

Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/11/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: Monensin is an antibiotic that can increase the feed efficiency of cattle production, but it is a toxic compound that can kill horses and make people sick. Previous work indicated that nisin, a bacteriocin approved for use in human food, could alter ruminal fermentations in a manner similar to monensin. Other workers had stated that "no nisin resistance has been reported," but our work demonstrated that the ruminal bacterium, Streptococcus bovis, could develop nisin resistance after only a short period of exposure. Nisin resistance would negate the use of nisin as a feed additive. Nisin resistance was due to an alteration in lipoteichoic acids, and this change also caused an increase in ampicillin resistance.

Technical Abstract: The growth of Streptococcus bovis JB1 was initially inhibited by nisin (1 uM), but these nisin-treated cultures eventually grew as rapidly as untreated cultures. When individual colonies from an untreated agar plate were transferred to basal medium containing 1 uM nisin, all of the cultures became nisin-resistant. Based on these results, it appeared that nisin resistance was a generalized induction rather than a selection per se. Non-induced, glucose-energized cells lost virtually all of their intracellular potassium if 1 uM was added, but induced cells retained potassium after 10 uM nisin was added. Induced cultures remained nisin-resistant even if nisin was not present, but competition studies indicated that non-induced cells could displace induced ones if nisin was not present. Isolates obtained from the rumen were initially as nisin-sensitive as non-induced S. bovis JB1 cultures, but they also developed nisin resistance. Nisin-resistant S. bovis JB1 cultures were still sensitive to monensin, tetracycline, vancomycin and bacitracin, but ampicillin resistance was 1000-fold greater. Nisin-induced cells were less hydrophobic and more lysozyme-resistant than non-induced cells. Because the nisin-induced cells bound less cytochrome c, it appeared that nisin was being excluded by a net positive (less negative) charge. Nisin-resistant cells had more lipoteichoic acid than uninduced cells. De-esterified lipoteichoic acids from nisin-resistant cells migrated more slowly through a polyacrylamainde gel than those from non-induced cells. These results indicated that lipoteichoic acids could be modified to increased the resistance of Streptococcus bovis to nisin.