Nisin Resistance of Streptococcus bovis

Abstract

The growth of Streptococcus bovis JB1 was initially inhibited by nisin (1 M), and nisin caused a more than 3-log decrease in viability. However, some of the cells survived, and these nisin-resistant cells grew as rapidly as untreated ones. To see if the nisin resistance was merely a selection, nisin-sensitive cells were obtained from agar plates lacking nisin. Results indicated that virtually any nisin-sensitive cell could become nisin-resistant if the ratio of nisin to cells was not too high and the incubation period was long enough. Isolates obtained from the rumen were initially nisin sensitive, but they also developed nisin resistance. Nisin-resistant cultures remained nisin resistant even if nisin was not present, but competition studies indicated that nisin-sensitive cells could eventually displace the resistant ones if nisin was not present. Nisin-sensitive, glucose-energized cells lost virtually all of their intracellular potassium if 1 M nisin was added, but resistant cells retained potassium even after addition of 10 M nisin. Nisin-resistant cells were less hydrophobic and more lysozymeresistant than nisin-sensitive cells. Because the nisin-resistant cells bound less cytochrome c, it appeared that nisin was being excluded by a net positive (i.e., less negative) charge. Nisin-resistant cells had more lipoteichoic acid than nisin-sensitive cells, and deesterified lipoteichoic acids from nisin-resistant cells migrated more slowly through a polyacrylamide gel than those from nisin-sensitive cells. These results indicated that lipoteichoic acids could be modified to increase the resistance of S. bovis to nisin. S. bovis JB1 cultures were still sensitive to monensin, tetracycline, vancomycin, and bacitracin, but ampicillin resistance was 1,000-fold greater.Streptococcus bovis is a rapidly growing and opportunistic bacterium that is usually found at low numbers in the rumen, but its numbers can increase dramatically if cattle are switched abruptly from hay to grain diets. S. bovis produces lactate when carbohydrates are in excess, and lactate accumulation in the rumen can cause acidosis (31). Ruminal acidosis causes decreases in food intake and ruminal ulceration and founder, and it can even kill the animal (23, 31). S. bovis has also been implicated in the colon cancer of humans (9).Since the 1970s, the feed additive monensin has been used to modify ruminal fermentations, and this antibiotic is most effective against gram-positive bacteria (28). In vitro studies have indicated that monensin can inhibit S. bovis (21), but only higher than normal doses of monensin (approximately 350 mg/animal/day) could prevent S. bovis proliferation and acute ruminal acidosis (22). Recent work has indicated that nisin and monensin have similar effects on in vitro ruminal fermentations, but the effect of nisin on S. bovis has not been described (4).Nisin is a small peptide (34 amino acids) that forms pores in cell membranes, has "generally recognized as safe" (GRAS) status, and is approved for use as a food preservative (13,20...

Scorpion venom as antimicrobial peptides (AMPs): A review article

“…The resistance to AMPs by human pathogen is recently accepted as one of the microorganism virulence factors, bacterial strains resistant to AMPs also reported to be highly resistant to conventional antibiotics [43].…”

Distinct Effects of Bovicin HC5 and Virginiamycin on in vitro Ruminal Fermentation and Microbial Community Composition

“…Streptococcus equinus HC5 was routinely cultivated under anaerobic conditions (39 °C, 18 h) in basal medium as previously described by Mantovani and Russell (2001). Alicyclobacillus acidoterrestris DSMZ 2498 was cultivated (43 °C, 16 h) under aerobic conditions in BAM (Bacillus acidocaldarius medium) medium containing (per liter): 2.0 g yeast extract; 0.2 g (NH 4 ) 2 SO 4 ; 0.5 g MgSO 4 ·7H 2 O; 0.25 g CaCl 2 ·H 2 O; 3.0 g KH 2 PO 4 and 5.0 g glucose.…”

The Expanding Role of Lipid II as a Target for Lantibiotics

“…It has been shown that many nisin-sensitive Grampositive bacteria, including clinically relevant strains, can acquire nisin resistance upon repeated exposure to increasing nisin concentrations [10,44,94,95]. This type of resistance is often lost once nisin pressure is removed [10] and is more accurately described as a physiological adaptation, although the nisin resistance of Streptococcus bovis was claimed to be stable, resistant cells were rapidly overgrown by sensitive ones [94]. Unlike vancomycin resistance, this adaptive mechanism does not involve an alteration of either the structure or quantity of lipid II.…”

“…Unlike vancomycin resistance, this adaptive mechanism does not involve an alteration of either the structure or quantity of lipid II. Rather, lipid II is effectively 'shielded' from nisin by a change in the cell-wall composition [10,94,[96][97][98][99]. Normally, the cell wall of a Gram-positive bacterium is highly negatively charged due to the phosphate groups of teichoic acid, another major component of the cell wall (Figure 12).…”