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Increased activity of 16-membered lactone ring macrolides against erythromycin-resistant Streptococcus pyogenes and Streptococcus pneumoniae: characterization of South African isolates.

The susceptibility of 40 erythromycin-resistant isolates of Streptococcus pyogenes and 40 multiply-resistant isolates of Streptococcus pneumoniae to six macrolide antibiotics, representing 14-, 15- and 16-membered lactone ring structures, was tested. The genetic basis for macrolide resistance in the strains was also determined. Both erm and mef determinants were encountered in the 36 S. pneumoniae isolates tested, but only mef in the five S. pyogenes isolates tested. All isolates showed cross-resistance among the 14-membered macrolides erythromycin, clarithromycin and roxithromycin and the 15-membered macrolide, azithromycin. However, the erythromycin-resistant S. pyogenes isolates retained full susceptibility to spiramycin and josamycin (16-membered agents). These latter two antibiotics were also more active than the other macrolides against erythromycin-resistant S. pneumoniae isolates, especially josamycin which was 8-64 times more active than erythromycin; spiramycin was only two to eight times more active than erythromycin.

Anti-Bacterial Agents↗

In vitro activity of ketolides telithromycin and HMR 3004 against italian isolates of Streptococcus pyogenes and Streptococcus pneumoniae with different erythromycin susceptibility.

Two ketolides, telithromycin and HMR 3004, were evaluated for their in vitro activity against erythromycin-susceptible and -resistant strains of Streptococcus pyogenes and Streptococcus pneumoniae. On the basis of their resistance to macrolide, lincosamide and streptogramin (MLS) antibiotics, erythromycin-resistant test strains were assigned to the constitutive resistance (cMLS) phenotype, the inducible resistance (iMLS) phenotype or the M phenotype. iMLS S. pyogenes strains were further subdivided into the three recently described subtypes iMLS-A, -B and -C. Telithromycin and HMR 3004 were uniformly and highly active against pneumococci (regardless of their susceptibility or resistance to erythromycin and/or penicillin), erythromycin-susceptible S. pyogenes and erythromycin-resistant S. pyogenes strains of the M phenotype (in which resistance is mediated by an efflux system) or iMLS-B or -C phenotype (in which resistance is mediated by a methylase encoded by the ermTR gene). Both ketolides were less active against erythromycin-resistant S. pyogenes strains with the cMLS phenotype or the iMLS-A subtype (where resistance is mediated by a methylase encoded by the ermAM gene), these strains ranging in phenotype from the upper limits of susceptibility to low-level resistant.

Anti-Bacterial Agents↗

Detection of macrolide resistance mechanisms in Streptococcus pneumoniae and Streptococcus pyogenes using a multiplex rapid cycle PCR with microwell-format probe hybridization.

In this study, a multiplex rapid cycle PCR with microwell-format probe hybridization method was developed to perform high-volume screening for macrolide resistance determinants in isolates of Streptococcus pneumoniae and Streptococcus pyogenes. The method was then utilized to determine the distribution of macrolide resistance mechanisms in recent isolates of S. pneumoniae and S. pyogenes from Great Britain and Ireland. For 83 strains of macrolide resistant S. pneumoniae tested, 51 (61.4%) were positive for mef(A), 29 (34.9%) erm(B), two (2.4%) double mechanisms mef(A) + erm(B), and one (1.2%) negative for all mechanisms tested. For 56 strains of macrolide-resistant S. pyogenes tested, 33 (58.9%) were positive for erm(A) subclass erm(TR), 18 (32.1%) mef(A) and five (8.9%) erm(B).

Anti-Bacterial Agents↗

Molecular characterization of macrolide resistance mechanisms among Streptococcus pneumoniae and Streptococcus pyogenes isolated from the PROTEKT 1999-2000 study.

In this study, the distribution of macrolide resistance mechanisms was determined for isolates of Streptococcus pneumoniae and Streptococcus pyogenes obtained from the PROTEKT 1999-2000 study (a global, longitudinal study of the antibacterial susceptibility of bacterial pathogens associated with community-acquired lower respiratory tract infections). The global macrolide resistance mechanism distribution results for 1043 macrolide-resistant S. pneumoniae isolates collected from 25 countries were as follows: 35.3% mef(A), 56.2% erm(B), 6.8% both mef(A) and erm(B), 0.2% erm(A) subclass erm(TR) and 1.5% negative for mechanisms tested. Mechanisms of macrolide resistance were found to vary widely between countries and different geographical regions with mef(A) predominating in North America and erm(B) in Europe. Approximation of genotype from macrolide MIC without molecular determination of the mechanism of resistance resulted in an error of 10.2% (106 isolates). Overall, for 143 macrolide-resistant S. pyogenes isolates, 46.1% of the isolates tested were mef(A), 30.8% were erm(B), 23.1% were erm(A) subclass erm(TR) and no isolates were negative for all the genetic markers tested. Again, the distribution varied widely between countries and geographical regions. This study provides valuable baseline data for the continued monitoring of the evolution of macrolide resistance development in these important respiratory tract pathogens. The ketolide telithromycin retained excellent anti-pneumococcal activity irrespective of macrolide resistance mechanism, having a MIC(90) of 0.25, 0.5 and 0.5 mg/L against mef(A), erm(B) and mef(A)+erm(B) macrolide-resistant S. pneumoniae, respectively. It also exhibited potent activity against S. pyogenes that had become resistant to macrolides via either mef(A), (MIC(90 )0.5 mg/L) or erm(TR), (MIC(90) 0.03 mg/L).

Anti-Bacterial Agents↗

Antimicrobial susceptibility of Streptococcus pneumoniae, Streptococcus pyogenes and Haemophilus influenzae collected from patients across the USA, in 2001-2002, as part of the PROTEKT US study.

BACKGROUND: The PROTEKT US (Prospective Resistant Organism Tracking and Epidemiology for the Ketolide Telithromycin in the United States) surveillance programme was started in 2000, to chart the emergence and spread of antimicrobial resistance among isolates of Streptococcus pneumoniae, Streptococcus pyogenes and Haemophilus influenzae from across the USA. METHODS: In 2001-2002 (Year 2 of PROTEKT US) 242 centres from 46 states and the territory of Puerto Rico submitted a total of 10 012 S. pneumoniae, 4508 S. pyogenes and 3296 H. influenzae isolates from community-acquired respiratory tract infections (CARTIs). Susceptibility testing was performed and interpreted using NCCLS methodology and criteria. RESULTS: Overall, 35.4% of S. pneumoniae were non-susceptible to penicillin (14.2% intermediate, MIC 0.12-1 mg/L; 21.2% resistant, MIC > or =2 mg/L) and 27.9% were resistant to erythromycin (MIC > or =1 mg/L) (0.2% intermediate, MIC 0.5 mg/L). A total of 105 (1.0%) isolates were resistant to levofloxacin (MIC > or =8 mg/L). More than 99.2% of isolates were susceptible to telithromycin (MIC < or =1 mg/L) irrespective of penicillin and/or erythromycin resistance. All S. pyogenes isolates were susceptible to penicillin (MIC < or =0.12 mg/L) and 5.7% were resistant to erythromycin (MIC > or =1 mg/L) (0.3% intermediate, MIC 0.5 mg/L). The MIC90 of telithromycin for S. pyogenes was 0.03 mg/L. A total of 27.5% of H. influenzae isolates were beta-lactamase producers. Overall, 27.8% were resistant (MIC > or =4 mg/L) and 1.1% were intermediate to ampicillin (MIC 2 mg/L). A total of 96.3% of H. influenzae isolates were susceptible to telithromycin (MIC < or =4 mg/L). CONCLUSIONS: Antimicrobial resistance continues to be a problem in the USA. The ketolide telithromycin continues to show high activity against common CARTI pathogens, including those resistant to beta-lactams and macrolides.

Anti-Infective Agents↗

Activity of the new quinolones WCK 771, WCK 1152 and WCK 1153 against clinical isolates of Streptococcus pneumoniae and Streptococcus pyogenes.

OBJECTIVES AND METHODS: The new fluoroquinolones WCK 771, WCK 1152 and WCK 1153 were developed to overcome quinolone resistance in Gram-positive bacteria. The activity of these new quinolones was tested against 159 clinical isolates of Streptococcus pneumoniae and 52 clinical isolates of Streptococcus pyogenes using the microbroth dilution method. RESULTS: MIC50/MIC90 values (mg/L) of WCK 771, WCK 1152 and WCK 1153 for quinolone-susceptible S. pneumoniae (n = 119; 54 penicillin G-susceptible, 53 penicillin G-intermediate, and 12 penicillin G-resistant strains) were 0.25/0.5, 0.03/0.06 and 0.016/0.03, respectively. MIC50/MIC90 values (mg/L) for quinolone-resistant pneumococci (n = 40) increased to 4/16, 0.25/1 and 0.125/0.5, respectively. Against S. pyogenes, WCK 771, WCK 1152 and WCK 1153 were also highly active with MIC50/MIC90 values (mg/L) of 0.25/0.25, 0.03/0.06 and 0.03/0.03, respectively. CONCLUSIONS: Overall, WCK 771 was highly active against quinolone-susceptible, but not against quinolone-resistant S. pneumoniae, whereas WCK 1152 and WCK 1153 were more potent and were able to overcome quinolone resistance in both S. pneumoniae and S. pyogenes.

Anti-Bacterial Agents↗

Interruption of the Streptococcus gordonii M5 sspA/sspB intergenic region by an insertion sequence related to IS1167 of Streptococcus pneumoniae.

Streptococcus gordonii M5 and DL1 each express two related adhesin polypeptides, SspA and SspB, which are members of the antigen I/II family of streptococcal surface proteins. The sspA and sspB genes are tandemly arranged in both strains, with sspA residing upstream of sspB. The genes are separated by approximately 400 nucleotides in S. gordonii DL1 and 1300 nucleotides in S. gordonii M5. The nucleotide sequence of the sspA/sspB intergenic region of strain M5 is reported and the difference in length compared to S. gordonii DL1 shown to arise from the presence of an insertion sequence, designated ISSg1, consisting of 1197 bp. The nucleotide sequence of ISSg1 is highly homologous to IS1167 to Streptococcus pneumoniae and is related to a lesser extent to other members of the IS1096 family of bacterial insertion sequences. It contains a single ORF of 1026 bp, encoding a putative transposase polypeptide of 342 amino acids. The deduced transposase sequence exhibits 93% identity with the transposase polypeptides encoded by IS1167. However, the S. gordonii protein lacks a 90 residue central domain that is present in the IS1167 transposase and in the transposase polypeptides encoded by the related IS elements. In addition, the organization of the inverted repeats flanking the transposase gene in S. gordonii differs from IS1167. Extension products generated from a sspB-specific primer indicated that transcription initiates within the intergenic region in both S-gordonii strains, suggesting that sspA and sspB are independently transcribed. Transcription appears to initiate 42 bases upstream of sspB in S. gordonii DL1. In contrast, sspB transcription in M5 initiates at least 125 bases upstream of sspB, in close proximity to the terminal inverted repeat of ISsg1. These results indicate that the sspB promoter of S. gordonii M5 and DL1 are not conserved and suggest that ISSg1 sequences may play a role in directing the expression of sspB in S. gordonii M5.

Adhesins, Bacterial↗

Longitudinal study of dental caries incidence associated with Streptococcus mutans and Streptococcus sobrinus in pre-school children.

Streptococcus mutans and Streptococcus sobrinus are known to be associated with the development of dental caries. In this study these bacteria were detected in pre-school children (each with primary dentition, age range 3-5 years, n = 60) using a PCR method, and then their presence was compared with the incidence of dental caries over a 1-year period. Plaque samples were collected from all erupted tooth sites using a sterile toothbrush. Dental examinations at the beginning of the study (baseline) and after 1 year were also performed to determine decayed, missing, filled teeth (dmft) scores using WHO caries diagnostic criteria. The prevalences of S. mutans and S. sobrinus across all the subjects were 61.7% and 56.6%, respectively; 13 subjects (21.7%) were positive for S. mutans alone, 10 (16.6%) were positive for S. sobrinus alone and 24 (40.0%) were positive for both S. mutans and S. sobrinus, whereas 13 (21.7%) were negative for both S. mutans and S. sobrinus. dmft scores of subjects positive for both S. mutans and S. sobrinus at baseline and after 1 year were significantly higher than of those positive for S. mutans alone at the same stages (P < 0.01 and P < 0.001, respectively). The caries incremental increase was also significantly greater in those with both bacteria detected (P < 0.05). Our results indicate that pre-school children harbouring both S. mutans and S. sobrinus have a significantly higher incidence of dental caries than those with S. mutans alone.

Child, Preschool↗

Effect of inoculation sequence and nutrients upon Streptococcus mutans BHT and Streptococcus mitior LPA-1 growing on human teeth in an artificial mouth.

Human teeth in an artificial mouth were inoculated with Streptococcus mutans BHT, Streptococcus mitior LPA-1, or sequentially with both organisms. Incubation was continued for 90 h. Mixed populations were largest when a nutrient supplement containing 5.0% (w/v) sucrose was supplied. Fewer organisms were recovered from experiments with synthetic saliva only, or when a supplement containing 0.05% (w/v) glucose was available. The inoculation sequence determined the total viable count and a larger population resulted when Strep. mutans was the initial colonizer (P less than 0.01). Strep. mutans was always able to become established even when super-infected on to a 24 h plaque of Strep. mitior. The final proportion of Strep mutans was lower when it was the superinfecting organism and the sucrose (P less than 0.01) or glucose (P less than 0.05) nutrient supplement was provided. This work confirms the importance of inoculation sequence and presence of sugars in plaque accumulation and demonstrates the fundamental role of microbial interactions in this process.

Ecology↗

Evolution of penicillin resistance in Streptococcus pneumoniae; the role of Streptococcus mitis in the formation of a low affinity PBP2B in S. pneumoniae.

Penicillin-resistant strains of Streptococcus pneumoniae possess forms of penicillin-binding proteins (PBPs) that have a low affinity for penicillin compared to those from penicillin-sensitive strains. PBP genes from penicillin-resistant isolates are very variable and have a mosaic structure composed of blocks of nucleotides that are similar to those found in PBP genes from penicillin-sensitive isolates and blocks that differ by up to 21%. These chromosomally encoded mosaic genes have presumably arisen following transformation and homologous recombination with PBP genes from a number of closely related species. This study shows that PBP2B genes from many penicillin-resistant isolates of S. pneumoniae contain blocks of nucleotides originating from Streptococcus mitis. In several instances it would appear that this material alone is sufficient to produce a low affinity PBP2B. In other examples PBP2B genes possess blocks of nucleotides from S. mitis and at least one additional unidentified species. Mosaic structure was also found in the PBP2B genes of penicillin-sensitive isolates of S. mitis or S. pneumoniae. These mosaics did not confer penicillin resistance but nevertheless reveal something of the extent to which localized recombination occurs in these naturally transformable streptococci.

Amino Acid Sequence↗

Molecular basis of the optochin-sensitive phenotype of pneumococcus: characterization of the genes encoding the F0 complex of the Streptococcus pneumoniae and Streptococcus oralis H(+)-ATPases.

The gene responsible for the optochin-sensitive (OptS) phenotype of Streptococcus pneumoniae has been characterized. Sequence comparisons indicated that the genes involved encoded the subunits of the F0 complex of an H(+)-ATPase. Sequence analysis and transformation experiments showed that the atpC gene is responsible for the optochin-sensitive resistant (OptS/OptR) phenotype. Our results also show that natural as well as laboratory OptR isolates have arisen by point mutations that produce different amino acid changes at positions 48, 49 or 50 of the ATPase c subunit. The nucleotide sequence of the F0 complex of the Streptococcus oralis ATPase has also been determined. In addition, comparison of the sequence of the atpCAB genes of S. pneumoniae R6 (OptS) and M222 (an OptR strain produced by interspecies recombination between pneumococcus and S. oralis), and S. oralis revealed that, in M222, an interchange of atpC and atpA had occurred. We also demonstrate that optochin specifically inhibited the membrane-bound ATPase activity of the S. pneumoniae wild-type (OptS) strains, and found a 100-fold difference between OptS and OptR strains, both in growth inhibition and in membrane ATPase resistance.

Amino Acid Sequence↗

Effect of a bacteriocin-producing strain of Streptococcus sobrinus on infection and establishment of Streptococcus mutans on tooth surfaces in rats.

The effect of bacteriocin produced by Streptococcus sobrinus MT6223 on infection and establishment of Streptococcus mutans MT6222 was studied in specific pathogen-free rats. These strains were isolated from a carious lesion of a single subject. S. mutans MT6222 was found to be susceptible to the growth inhibitory action of S. sobrinus MT6223. When simultaneously inoculated into the oral cavity of rats, even a small inoculum (10(5) CFU) of S. sobrinus MT6223 completely inhibited colonization of S. mutans MT6222 on the tooth surface. Also, S. sobrinus MT6223 eliminated S. mutans MT6222 when MT6223 (10(8) CFU) was inoculated 2 days after the inoculation of 10(8) CFU cells of MT6222. Similar results were obtained in dental plaque samples from the tooth surface and the fissures of the upper molars at the end of the experiment. However, when S. sobrinus MT6223 (10(8) CFU) was inoculated 2 weeks after the inoculation of S. mutans MT6222 (10(8) CFU), MT6223 coexisted with MT6222. However, the plaque samples showed that MT6223 inhibited the establishment of MT6222 on smooth surfaces, but not in fissures. In addition, MT6223 protected against subsequent infection with MT6222. However, a nonbacteriocinogenic mutant of S. sobrinus MT6223 did not inhibit the infection and establishment of S. mutans MT6222.

Animals↗

Maintenance of proton motive force by Streptococcus mutans and Streptococcus sobrinus during growth in continuous culture.

The components of the transmembrane electrochemical proton gradient, or proton motive force (PMF, delta p), were determined in cells of Streptococcus mutans Ingbritt and Streptococcus sobrinus ATCC 27352 growing in continuous culture under conditions of changing glucose concentration, growth rate and growth pH. The pH gradient (delta pH) and membrane electrical potential (delta psi) were assayed with the weak acid, salicyclic acid, and the lipophilic cation, methyltriphenylphosphonium iodide, respectively. S. mutans Ingbritt growing in continuous culture (pH 7.0, dilution rate (D) = 0.1 h-1) at 8 glucose concentrations ranging from 2.8 to 288 mM maintained a relatively constant delta p of 58.3 mV (SD +/- 5.8) in spite of a transition from glucose to nitrogen-limited growth and significant changes in cell physiology. Changes included a decreasing yield constant, increasing glucose uptake rates in the chemostat, repression of Ellglc of the PEP phosphotransferase sugar transport system and decreasing glycolytic capacity of the cells as the medium glucose concentration increased. Changes in the dilution or growth rate of S. mutans Ingbritt from 0.1 to 1.0 h-1 and S. sobrinus from 0.1 to 0.8 h-1, when growing at pH 7.0 with limited glucose and lactose, respectively, resulted in significantly lower delta p values due to the dissipation of the delta psi. When the cells of S. mutans Ingbritt were grown with excess glucose (nitrogen limitation), lower delta p values were observed at pH 5.5, but not at pH 7.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗

Metabolism of 17 beta-estradiol by oral Streptococcus mutans, Streptococcus sanguis, Bacillus cereus and Candida albicans.

The ability of oral isolates of Streptococcus mutans, Streptococcus sanguis, Bacillus cereus and Candida albicans to metabolize 17 beta-estradiol was analyzed by thin-layer chromatography using 4-14C-estradiol as the substrate. All test microorganisms metabolized 17 beta-estradiol. Estrone was the main metabolic product, except for B. cereus, which converted 17 beta-estradiol mainly to unidentified, more polar metabolites. S. sanguis and B. cereus had the most active metabolism but S. mutans and C. albicans were also active.

Bacillus cereus↗

Antimicrobial susceptibility of 1042 strains of Streptococcus mutans and Streptococcus sobrinus: comparison from 1985 to 1989.

A total of 1042 strains of Streptococcus mutans and Streptococcus sobrinus isolated between 1985 and 1989 were tested to study the evolution of their sensitivity to penicillin, amoxycillin, amoxycillin/clavulanic acid, cefuroxime, tetracycline, erythromycin, spiramycin, acetyl spiramycin, lincomycin and clindamycin. The strains were taken from stock cultures and isolated from human saliva and dental plaque. The minimal inhibitory concentration (MIC) was determined by an agar dilution method. Except for spiramycin and acetyl spiramycin, all the antibiotics inhibited 100% of the strains with concentrations less than or equal to 2 micrograms/ml. Microorganisms from both species underwent a slow progressive loss of sensitivity to all the antibiotics over a 5-year period of study, showing statistically significant results in most cases.

Dental Plaque↗

Selective effects of histidine-rich polypeptides on the aggregation and viability of Streptococcus mutans and Streptococcus sanguis.

Enriched preparations of histidine-rich polypeptides (HRPs) and isolated HRP pairs (1-2, 3-4 and 5-6) degrade in the presence of fresh autologous whole saliva to a series of low-molecular-weight cationic peptides (HRPs 6a-c and 7). Analysis of the HRPs during degradation indicates that: HRP 1 is not the parent molecule of the HRPs; the HRP pairs do not convert to each other in a cascade-like sequence in saliva; and the HRPs can be separated into 2 groups consisting of HRPs 1-2 and 3-7. Preparations containing HRPs 1-7, 1-2, and 3-7 were obtained by fractionation and separation on Bio-Rex 70, and tested for aggregating and antibacterial effects against Streptococcus mutans BHT, S. mutans GS-5 and Streptococcus sanguis G9B. HRPs 1-2 had significant aggregating effects on all 3 strains but the other HRPs had little to no agglutinating ability. The HRPs did not inhibit the growth of S. sanguis, and HRPs 1-2 enhanced its growth. No growth enhancement by the HRPs was observed for the 2 S. mutans strains. However, significant bacterial inhibition of the S. mutans strains was noted after incubation with HRPs 3-7. The data suggest that the dissimilar effects of HRPs 1-2 and 3-7 may be of importance in the colonization and growth of S. mutans and S. sanguis in vivo.

Bacterial Adhesion↗

Antineoplastic agents inhibit the growth of Streptococcus mutans and Streptococcus sanguis in vitro.

The effect of methotrexate (MTX) and doxorubicin on the growth, metabolism and ultrastructure of Streptococcus mutans and Streptococcus sanguis was studied in vitro. Both anticancer drugs exerted an inhibitory effect on the oral streptococci. MTX was more inhibitory than doxorubicin. The minimum inhibitory concentrations (MICs) of MTX to S. mutans were 0.25-2.5 micrograms/ml and that of doxorubicin 0.2 mg/ml. The MICs of MTX and doxorubicin to S. sanguis were 0.025 micrograms/ml and 2.0-0.02 mg/ml, respectively. When saliva samples of patients with malignant tumors receiving various doses of MTX were analyzed, MTX was found to be secreted into the oral cavity at concentrations ranging from 0.014 to 4.486 micrograms/ml. The saliva of these patients was also found to inhibit the growth of S. mutans, and the inhibition zones were in accordance with the MIC values observed. The results suggest that anticancer therapy must be taken into account when the salivary microbiological findings of cancer patients are interpreted.

Adult↗

Differential toxic effects of lactate and acetate on the metabolism of Streptococcus mutans and Streptococcus sanguis.

Experiments were conducted with Streptococcus mutans NCTC 10449 and Streptococcus sanguis ATCC 10556 to determine whether the acid end-products, lactate and acetate, were involved in the regulation of cellular growth and metabolism. The growth rate and culture biomass of both organisms was inhibited by the addition of lactate and acetate at concentrations as high as 200 mM to the cultures, although the final pH values of the lactate and acetate cultures were similar. In addition, the metabolic conversion of glucose to lactate was decreased by external lactate but stimulated by acetate. In spite of this, calculation of the yield of cell biomass per mole of ATP (YATP) showed that the yield of both organisms actually increased in the presence of added lactate, but decreased with acetate. This indicates that the two acids interacted with the cells of the organisms by different mechanisms. For both organisms, the final external undissociated lactic acid was relatively constant at concentrations between 0 and 200 mM added lactate, 24.9-32.5 mM for S. mutans and 8.0-11.5 mM for S. sanguis. On the other hand, the final concentration of undissociated acetic acid in the S. mutans cultures increased from 2.9 to 83.7 mM as the medium acetate concentration increased, and from 1.0 to 36.0 mM with the S. sanguis cultures. Counterflow experiments provided evidence for a lactate carrier in both S. mutans and S. sanguis, but an acetate carrier in these organisms could not be demonstrated. [14C]-lactate and [14C]-acetate were taken up into de-energized, chemostatgrown cells of S. mutans and S. sanguis in response to an artificially generated pH gradient but not by an imposed electrical gradient. Thus, under these conditions lactate uptake occurred via a symport process with only one proton. Growth of both organisms in the presence of increasing concentrations of acetate resulted in a small reduction (27%) in the transmembrane pH gradient (delta pH) as measured by the permeant acid, [14C]-salicylate. However, the uptake of [14C]-acetate for the estimation of delta pH revealed significant inhibition of the acetate concentration gradient in the presence external acetate, indicating that the cells expelled the acetate anion. The results indicate that, unlike acetate uptake, lactate transport by S. mutans and S. sanguis was strictly regulated via the lactate carrier in order to prevent excessive dissipation of the pH gradient. Clearly, the formation of acetate by oral streptococci is more problematic for cellular homeostasis than the formation of lactate.

Acetic Acid↗