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PubMed1983

Specificity of cellular interaction in Streptococcus mitis ATCC 903. Inhibition of aggregation by carbohydrates.

To demonstrate the specificity of cellular interaction in the spontaneous aggregation of Streptococcus mitis ATCC 903 the inhibitory effect of various sugars was studied. More than 90% inhibition was recorded in 0.1 M concentrations of D-glucosamine, D-galactosamine and D-mannosamine. A reduction of the inhibition by more than 50% was observed when the N-acetylated derivatives of the hexosamines were tested. Polymers containing hexosamines such as hyaluronic acid, heparin and fetuin were potent inhibitors, in contrast to dextrans of different molecular weights. Inhibition was less than 20% in lactose, melibiose, cellobiose, methyl beta-D-galactopyranoside and a number of other sugars tested in 0.1 M concentration. The bacteria retained their ability to aggregate after removal of the inhibitory sugars by washing in phosphate buffer. These findings support the hypothesis that the specific nature of the spontaneous aggregation of S.mitis ATCC 903 depends on a lectin-ligand type interaction.

Adhesiveness↗

PubMed1982

Glucose uptake by Streptococcus mutans, Streptococcus mitis, and Actinomyces viscosus in the presence of human saliva.

Glucose uptake was examined by using whole-cell suspensions of Streptococcus mutans (strains BHT, Ingbritt, and GS-5), Streptococcus mitis (strains 9811 and 72x41), and Actinomyces viscosus (strains T6 and WVU626) incubated for up to 90 min in 0 to 82% (vol/vol) human whole salivary supernatant. Glucose uptake by the S. mutans strains was completely inhibited at all saliva concentrations. Dithiothreitol (DTT), present during saliva incubation, prevented saliva inhibition. Glucose uptake was also restored when saliva-inhibited cells were subsequently exposed to DTT. The inclusion of catalase in the saliva incubation mixtures resulted in protection equal to that obtained with DTT. The S. mitis strains were also inhibited by saliva but to a far lesser extent that S. mutans. DTT and catalase also protected S. mitis from saliva inhibition. Both A. viscosus strains were completely refractory to saliva inhibition of glucose uptake. Based on (i) the sensitivity of the catalase-negative streptococci and the resistance of catalase-positive actinomyces to saliva inhibition and (ii) the equal and complete protection to saliva inhibition afforded by DTT and catalase, we conclude that the lactoperoxidase-SCN(-)-H(2)O(2) system in saliva was the only antibacterial system expressed under our experimental conditions. The relative resistance of S. mitis 9811 (compared with S. mutans BHT) to saliva inhibition was shown not to result from poor H(2)O(2) production in either glucose-supplemented buffer or saliva solutions. S. mitis produced inhibitory quantities of H(2)O(2) that equaled or exceeded S. mutans H(2)O(2) accumulation. It is suggested that S. mitis might possess a greater ability to repair lactoperoxidase-mediated damage than does S. mutans. Every organism studied exhibited a saliva concentration-dependent, cell growth-independent stimulation of glucose uptake after 60 to 90 min of incubation. The A. viscosus and S. mitis strains showed saliva stimulation (or stabilization) of glucose uptake with unsupplemented saliva. In the case of S. mutans, saliva stimulation was only observed when DTT was present. The possible role of salivary lactoperoxidase as a modulator of the intraoral site specificities exhibited by S. mutans is discussed.

Actinomyces↗

PubMed1985

Binding of lectins to Streptococcus mitis cells. Studies of the specificity of ligand mediated aggregation.

Previous studies have shown that the mechanism of spontaneous aggregation of Streptococcus mitis ATCC 903 depends on a lectin-ligand type interaction. To study the specificity of the ligand, the binding of a number of lectins of different sugar specificities to the surface of untreated, trypsin and beta-galactosidase-treated bacteria was studied by assessing aggregation. Untreated bacteria were rapidly aggregated by concanavalin A (Con A), wheat-germ agglutination (WGA) and helix pomatia lectin (HPL). Other lectins tested, e.g. peanut agglutinin and soy bean lectin, did not induce aggregation. Lectin-induced aggregation was distinguished from the spontaneous one by recording the course of aggregation and inhibition of lectins by specific sugars. Trypsin-treated bacteria lost their ability for both spontaneous and lectin-induced aggregation. beta-galactosidase-treated bacteria were aggregated only in the presence of Con A and HPL. The bacteria retained their ability for spontaneous aggregation after removal of lectins and inhibitory sugars. These findings suggest that ligand is of glycoprotein nature, since it was removed from the bacterial surface by treatment with trypsin, as shown by the inability of treated cells for both spontaneous and lectin-induced aggregation. Partial degradation of the carbohydrate part of the ligand is indicated by the ability of beta-galactosidase-treated bacteria to aggregate in the presence of Con A and HPL.

Adhesiveness↗

PubMed1996

Clonal diversity of Streptococcus mitis biovar 1 isolates from the oral cavity of human neonates.

The clonal diversity of 101 isolates of the pioneer bacterium Streptococcus mitis biovar 1 obtained from the oral cavities of 40 human neonates 1 to 3 days, 2 weeks, and 1 month postpartum was examined by using rRNA gene restriction patterns. There was a high degree of genetic diversity, with the 101 isolates comprising 93 unique PvuII ribotypes. There were eight identical pairs of ribotype patterns, and seven of the eight pairs were obtained from individual neonates. Only one identical pair comprised isolates obtained from different neonates. In all but two cases, isolates with matching ribotypes were obtained at one visit. Two pairs of isolates with matching ribotype patterns were obtained from neonates on successive visits. The ribotype patterns of the isolates were examined by cluster analysis. The isolates forming each cluster were very similar, yet each cluster was well separated from its neighbors. When several isolates were obtained from individual neonates at a particular visit, in some instances they were contained in a single cluster, whereas in other cases each isolate was contained in a separate cluster. Isolates obtained from individual neonates on successive visits tended to be contained in different clusters. This high degree of diversity, which has been observed in other mucosal commensal bacteria, may serve as a mechanism for avoiding immune elimination of these bacteria.

Cloning, Molecular↗

PubMed2003

Major outbreak of toxic shock-like syndrome caused by Streptococcus mitis.

Severe illness caused by viridans streptococci rarely occurs in immunocompetent hosts. Between December 1990 and May 1991, thousands of patients in the YangZi River Delta area of Jiangsu Province, China, suffered from scarlet fever-like pharyngitis. Fewer cases occurred in subsequent years with the same seasonality. Approximately half of the cases developed complications characteristic of streptococcal toxic shock-like syndrome (TSLS). Throat cultures yielded predominant growth of alpha-hemolytic streptococci. All cases admitted to Haian People's Hospital were investigated. Clinical specimens were collected, medical records were reviewed, and bacterial isolates were identified phenotypically and analyzed by 16S rRNA gene sequencing and pulsed-field gel electrophoresis (PFGE). Proteins were purified from culture supernatants by extraction, ammonium sulfate precipitation, and fast-protein liquid chromatography. Biological activities of protein components were determined by subcutaneous inoculation into rabbits. A total of 178 cases of non-beta-hemolytic streptococcal scarlet fever-like pharyngitis were studied. In 88 (79.3%) of 111 patients, oropharyngeal swab cultures grew morphologically identical alpha-hemolytic streptococci. A protein in culture supernatants was pyrogenic in rabbits, was mitogenic for splenocytes, and enhanced rabbit susceptibility to endotoxin challenge. The N-terminal amino acid sequence of this 34-kDa protein showed no homology with known Streptococcus pyrogenic exotoxins. The organism was identified as Streptococcus mitis based on biochemical and 16S rRNA sequence analyses. Representative outbreak isolates from 1990 to 1995 displayed identical PFGE patterns. This TSLS outbreak in southeastern China was caused by a toxigenic clone of S. mitis. An apparently novel toxin may explain the unusual virulence of this organism.

Animals↗

PubMed2002

Successful treatment of meningitis caused by highly-penicillin-resistant Streptococcus mitis in a leukemic child.

In recent years, viridans streptococci have been reported with increasing frequency to cause infections in neutropenic cancer patients. Streptococcus mitis, one of the species included among viridans streptococci, is the most resistant to beta-lactam antibiotics in this group. Bacterial meningitis presenting without pleocytosis in the cerebrospinal fluid (CSF) is rare, and this situation could be confusing to physicians. It is also an uncommon infectious complication in leukemic patients with neutropenia. In patients with leukopenia caused by myelosuppression after chemotherapy, bacterial meningitis must be considered a possibility when a patient develops meningeal signs, even if no pleocytosis is found in the CSF. We report on a 6-year-old boy with leukemia and neutropenia who developed sepsis and meningitis caused by S. mitis with high-level resistance to penicillin and cephalosporins (MIC of both, >2 mg/l); he was a long-term survivor receiving chronic trimethoprim-sulfamethoxazole prophylaxis. The patient was successfully treated with a combination of vancomycin, ceftriaxone, and granulocyte-colony-stimulating factor.

Bacteremia↗

PubMed1990

Septicemia due to Streptococcus mitis in neutropenic patients with acute leukemia.

Eight neutropenic patients with acute lymphocytic or nonlymphocytic leukemia had septicemia due to different strains of Streptococcus mitis (St. mitis), a microorganism not commonly recognized as a special pathogen in leukemic patients. Four of the patients had been treated with high-dose cytosine arabinoside as part of the cytostatic regimen, six had a central venous line and four patients had oral lesions prior to the infection. Selective gut decontamination consisted of co-trimoxazole/colistin in five patients and quinolones in three patients. The first three patients died, either due to interstitial pneumonia with the adult respiratory distress syndrome (ARDS), or due to infection-triggered disseminated intravascular coagulation despite prompt empiric antibiotic therapy including vancomycin. The other patients improved after empiric supplementation of penicillin G (30 Mega/day) to the antibiotic regimen. Beginning ARDS in two of these patients dramatically responded to high-dose steroids. We conclude that St. mitis is a major pathogen in neutropenic leukemic patients. Infection appears to occur independently of acute leukemic cell type, regimen of selective gut decontamination, venous access, visible oral lesions or treatment with high-dose cytosine arabinoside. The clinical course of our patients raises questions about the value of commonly recommended empiric antibiotic regimens, which were clearly ineffective to control infections with St. mitis in this patient group. Our data indicate that immediate antibiotic therapy with penicillin G is indicated and may be life-saving for suspected St. mitis infections in neutropenic leukemic patients.

Adult↗

PubMed1996

Streptococcus mitis cell walls and lipopolysaccharide induce lethality in D-galactosamine-sensitized mice by a tumor necrosis factor-dependent pathway.

Purified cells walls of Streptococcus mitis induced tumor necrosis factor in vitro in whole blood of both lipopolysaccharide (LPS)-sensitive OF1 and LPS-resistant C3H/HeJ mice. They were as effective as heat-killed bacteria in inducing death in both strains of mice sensitized with D-galactosamine. Lethality was suppressed by anti-tumor necrosis factor antibodies. The histopathophysiological findings in mice after challenge with LPS or gram-positive cell walls were indistinguishable.

Animals↗

PubMed1996

[Purification and partial characterization of a novel human platelet aggregation factor in the extracellular products of Streptococcus mitis, strain Nm-65].

In this paper, we report the purification and partial characterization of human platelet aggregation factor form the extracellular products (ECP) of Streptococcus mitis (S. mitis) isolated from a patient with Kawasaki disease (KD). Platelet aggregation reaction was carried out using platelet-rich plasma (PRP) and washed platelets suspended in ACD-PBS. The aggregation factor was designated as S. mitis-derived human platelet aggregation factor (Sm-hPAF). The results obtained were as follows. 1) Sm-hPAF was isolated by chromatography on DEAE-Sepharose CL-6 B, hydroxyapatite and Superdex 75 columns. The purified Sm-hPAF showed a single band upon SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and molecular weight of approximately 66 kDa on SDS-PAGE. The isoelectric point (pI) of Sm-hPAF was 8.5, and Sm-hPAF showed an absorption peak at 278 nm on absorption spectra. When the platelet aggregation activity of the Sm-hPAF was compared with that of ECP, the specific aggregation activity of the of Sm-hPAF was significantly increased (up to 28-fold). Sugars were not found in Sm-hPAF. The sequence of the first 15 amino-terminal amino acid residues were H.Asp-Glu-Gln-Gly-Asn-Arg-Pro-Val-Glu-Thr-Glu-Asn-Ile-Ala-Arg. The platelet aggregation activity of Sm-hPAF was inactivated by heating at 45 degrees C for 10 min. 2) PGE2 was released from platelets after incubation for 10 min with Sm-hPAF in a dose-dependent fashion. Platelet aggregation by the Sm-hPAF was totally inhibited by either PGE1, or GRGDS, but these reagents did not inhibit the platelet aggregation by collagen. 3) Histological examination of the rabbit skin sites showing an early reaction revealed increased dilatation of the veins and capillaries with cellular infiltration in the perivascular space of the dermis. Hyperplasia of the endothelial cells was noted. Degeneration of the vascular walls was observed in the later stages of the reaction. Aggregation of red cells in the vascular endothelium was also observed. Sm-hPAF was capable of producing vasculitis. 4) Twenty (76.9%) platelet-rich plasma samples (PRP) derived from 26 healthy human volunteers reacted with Sm-hPAF, but the remaining 6 PRPs were not reactive. Preliminary study suggests the existence of an inhibitory factor in plasma from nonreactive donors.

Animals↗

PubMedDate not supplied

Penicillin-resistant Streptococcus mitis as a cause of septicemia with meningitis in febrile neutropenic children.

PURPOSE: The purpose of this report is to emphasize the importance of occurrence of Streptococcus mitis meningitis in febrile neutropenic children with hematopoietic malignancy. PATIENTS AND METHODS: Symptoms of meningitis and sepsis (fever, headache, changes in mental status) were seen in three patients who were severely neutropenic and undergoing cytotoxic chemotherapy for CNS relapse of their underlying malignancy (acute lymphoblastic leukemia (ALL), n = 2; Burkitt's lymphoma, n = 1). Chemotherapy had included cytosine arabinoside administered 7-14 days prior to presenting with sepsis and meningitis. All three patients had buccal mucositis or sinusitis. Blood cultures and CSF cultures showed S. mitis resistant to penicillin but sensitive to vancomycin. Vancomycin, at a dosage of 60 mg/kg/day to maximize CNS levels of antibiotic, was administered to all three children. RESULTS: Two of the patients recovered from S. mitis meningitis; recovery was associated with an improvement in their peripheral granulocyte counts. One patient, who remained neutropenic, died despite being treated with both intravenous and intraventricular vancomycin. CONCLUSION: Physicians caring for patients who are neutropenic and febrile need to be aware of the risk of meningitis occurring with S. mitis sepsis. Early treatment with high dosages of vancomycin (60 mg/kg/day) and an attempt to limit the duration of neutropenia are important factors in the outcome of such patients.

Bacteremia↗

PubMed2001

Diversity among clinical isolates of penicillin-resistant Streptococcus mitis: indication for a PBP1-dependent way to reach high levels of penicillin resistance.

A total of 12 non-epidemiologically related clinical isolates of Streptococcus mitis that showed different levels of resistance to penicillin were studied. Membrane-protein profiles and penicillin-binding protein (PBP) patterns showed a great polymorphism; and patterns of 4-7 PBPs, with sizes that ranged from approximately 101 kDa to approximately 40 kDa, were detected in each strain. No association could be found between PBP pattern and resistance level to penicillin among these isolates. Arbitrarily primed PCR confirmed the genetic diversity among this group of streptococci. One of the isolates of intermediate level of resistance to penicillin, which showed a PBP pattern similar to that of the high-resistance strains, was used as a laboratory model to analyse the mechanism underlying high-resistance acquisition by these strains. A 14-fold increase in penicillin resistance was obtained after a single selection step, which resulted in a decrease in penicillin affinity for PBP1. The size of this PBP (92 kDa) and the differences in PBP profiles of the penicillin-resistant clinical isolates suggest the existence in S. mitis of PBP-mediated mechanisms to acquire high-level resistance to penicillin, among which alterations in PBP1 seem to play a main role, in contrast to the PBP2X mediated mechanism described for other streptococci.

Bacterial Proteins↗

PubMed1983

Purification and characterization of two novel arginine aminopeptidases from Streptococcus mitis ATCC 9811.

Two novel aminopeptidases (I and II) which have specificity for amino-terminal arginine residues and strong sensitivity to divalent cations were purified from Streptococcus mitis ATCC 9811 by a procedure that involved treatment with a lytic enzyme for bacterial cell walls, followed by a series of chromatographies. Enzyme I was obtained as a homogeneous protein as judged by polyacrylamide gel electrophoresis and had a specific activity of 484.8 units per mg protein using L-arginine-2-naphthylamide as substrate; its Km value was 2.6 X 10(-5) M. The molecular weight was estimated to be 62,000, and its isoelectric point was pH 4.4. Enzyme II was purified to a specific activity of 128.0 units per mg protein and had a Km value of 3.8 X 10(-5) M. The molecular weight was estimated to be 360,000, and its isoelectric point was pH 5.7. The pH optima of enzymes I and II were 8.6 and 7.6, respectively. Both enzymes were inactivated by sulfhydryl reagents and metal ions but were markedly activated by EDTA. The chloride ion had an inhibitory rather than a stimulatory effect on the activity of both enzymes. Substrate specificity studies indicated that both the enzymes specifically hydrolyze N-terminal arginine residues from a-aminoacyl 2-naphthylamides and peptides, but they could not attack the L-arginyl-L-prolyl-peptide.

Aminopeptidases↗

PubMed1990

Streptococcus mitis sepsis in bone marrow transplant patients receiving oral antimicrobial prophylaxis.

PURPOSE: Streptococcal infection has increasingly become a problem in neutropenic patients. We report on an outbreak of Streptococcus mitis sepsis in six bone marrow transplant patients receiving oral antimicrobial prophylaxis. PATIENTS AND METHODS: We performed an epidemiologic study of all patients in our bone marrow transplant program from 1986 to 1988. The hospital and microbiology records for all patients were reviewed. All bone marrow patients were treated according to specified protocols, including an oral prophylactic antimicrobial regimen that was changed in late 1987 from vancomycin/polymyxin/tobramycin to norfloxacin. Identification, susceptibility testing, and whole cell protein analysis of streptococcal isolates were performed at the Reference and Antimicrobial Investigations Laboratories at the Centers for Disease Control. RESULTS: We detected six cases of S. mitis sepsis among 21 patients undergoing bone marrow transplantation. No other concurrent pathogen was isolated from any patient at the time of the S. mitis bacteremia. Bacteremia developed within 72 hours of transplant in five of six patients and was associated with severe mucositis in four patients. An environmental study failed to reveal any common source for the outbreak, and whole cell protein analysis of all six S. mitis isolates revealed each to be distinct. Of 12 patients receiving oral vancomycin/polymyxin/tobramycin, one developed S. mitis bacteremia, versus five of nine patients receiving norfloxacin (p less than 0.03). CONCLUSION: We believe S. mitis bacteremia is a potential complication of bone marrow transplantation and is associated with antimicrobial prophylaxis with norfloxacin, especially in the setting of mucositis.

Administration, Oral↗

PubMed1989

Uptake of 14C-xylitol by xylitol-cultured Streptococcus sobrinus ATCC 27352 and Streptococcus mitis ATCC 36249 in vitro.

The effect of three successive cultures in the presence of 6% xylitol on the uptake of 14C-xylitol was studied using resting cells of Streptococcus sobrinus ATCC 27352 and Streptococcus mitis ATCC 36249. In the case of S. mitis, the three successive cultures did not alter the growth inhibition observed in the presence of xylitol. In the case of S. sobrinus, however, growth inhibition decreased. The 14C-xylitol uptake experiments also demonstrated that uptake of xylitol by S. sobrinus was decreased by culture in the presence of xylitol. Previous 14C-xylitol uptake levels were, however, re-established by culturing S. sobrinus in the presence of glucose alone. Culture in the presence of xylitol did not affect 14C-xylitol uptake in the case of S. mitis. These results show that S. sobrinus and S. mitis differ in the ways they handle of exogenous xylitol, and that uptake of xylitol by S. sobrinus could be reversibly regulated by addition xylitol to the growth medium.

Cell Division↗

PubMed2001

Genetic loci of Streptococcus mitis that mediate binding to human platelets.

The direct binding of bacteria to platelets is a postulated major interaction in the pathogenesis of infective endocarditis. To identify bacterial components that mediate platelet binding by Streptococcus mitis, we screened a Tn916deltaE-derived mutant library of S. mitis strain SF100 for reduced binding to human platelets in vitro. Two distinct loci were found to affect platelet binding. The first contains a gene (pblT) encoding a highly hydrophobic, 43-kDa protein with 12 potential membrane-spanning segments. This protein resembles members of the major facilitator superfamily of small-molecule transporters. The second platelet binding locus consists of an apparent polycistronic operon. This region includes genes that are highly similar to those of Lactococcus lactis phage r1t and Streptococcus thermophilus phage 01205. Two genes (pblA and pblB) encoding large surface proteins are also present. The former encodes a 107-kDa protein containing tryptophan-rich repeats, which may serve to anchor the protein within the cell wall. The latter encodes a 121-kDa protein most similar to a tail fiber protein from phage 01205. Functional mapping by insertion-duplication mutagenesis and gene complementation indicates that PblB may be a platelet adhesin and that expression of PblB may be linked to that of PblA. The combined data indicate that at least two genomic regions contribute to platelet binding by S. mitis. One encodes a probable transmembrane transporter, while the second encodes two large surface proteins resembling structural components of lysogenic phages.

Amino Acid Sequence↗

PubMed2001

Proteins PblA and PblB of Streptococcus mitis, which promote binding to human platelets, are encoded within a lysogenic bacteriophage.

The binding of platelets by bacteria is a proposed central mechanism in the pathogenesis of infective endocarditis. Platelet binding by Streptococcus mitis strain SF100 (an endocarditis isolate) was recently shown to be mediated in part by the surface proteins PblA and PblB. The genes encoding PblA and PblB are clustered with genes nearly identical to those of streptococcal phages r1t, 01205, and Dp-1, suggesting that pblA and pblB might reside within a prophage. To address this possibility, cultures of SF100 were exposed to either mitomycin C or UV light, both of which are known to induce the lytic cycle of many temperate phages. Both treatments caused a significant increase in the transcription of pblA. Treatment with mitomycin C or UV light also caused a substantial increase in the expression of PblA and PblB, as detected by Western blot analysis of proteins in the SF100 cell wall. By electron microscopy, phage particles were readily visible in the supernatants from induced cultures of SF100. The phage, designated SM1, had a double-stranded DNA genome of approximately 35 kb. Southern blot analysis of phage DNA indicated that pblA and pblB were contained within the SM1 genome. Furthermore, Western blot analysis of phage proteins revealed that both PblA and PblB were present in the phage particles. These findings indicate that PblA and PblB are encoded by a lysogenic bacteriophage, which could facilitate the dissemination of these potential virulence determinants to other bacterial pathogens.

Base Sequence↗

PubMed1967

Metabolism of the reserve polysaccharide of Streptococcus mitis. Properties of alpha-(1-->6)-glucosidase, its separation from transglucosylase, and the action of the two enzymes on branched oligosaccharides.

1. An alpha-(1-->6)-glucosidase has been separated from cell extracts of Streptococcus mitis. The enzyme was freed from transglucosylase by adsorption of the latter on retrograded amylose. 2. The enzyme was detected in five of the six strains of S. mitis that were studied; alpha-(1-->6)-glucosidase was not found in strain RB1633, a strain that did not store polysaccharide. 3. The glucosidase could act on compounds in which alpha-glucose is joined through an alpha-(1-->6)-bond to either a maltosaccharide or an isomaltosaccharide. 6(2)-alpha-Glucosylmaltose (panose) and 6(3)-alpha-glucosylmaltotriose were hydrolysed more rapidly and isomaltodextrins more slowly than isomaltose. 4. Transferring activity towards isomaltose and panose was appreciable when the concentration of substrate was 2% or higher. 5. The enzyme had no action on alpha-(1-->4)-glucosidic linkages. 6-alpha-Maltodextrinylglucoses were hydrolysed only after transglucosylase action had attenuated them to isomaltose.

Journal Article↗

PubMed2000

Inhibition of Streptococcus mutans NS adhesion to glass with and without a salivary conditioning film by biosurfactant- releasing Streptococcus mitis strains.

The release of biosurfactants by adhering microorganisms as a defense mechanism against other colonizing strains on the same substratum surface has been described previously for probiotic bacteria in the urogenital tract, the intestines, and the oropharynx but not for microorganisms in the oral cavity. Two Streptococcus mitis strains (BA and BMS) released maximal amounts of biosurfactants when they were grown in the presence of sucrose and were harvested in the early stationary phase. The S. mitis biosurfactants reduced the surface tensions of aqueous solutions to about 30 to 40 mJ m(-2). Biochemical and physicochemical analyses revealed that the biosurfactants released were glycolipids. An acid-precipitated fraction was extremely surfactive and was identified as a rhamnolipidlike compound. In a parallel-plate flow chamber, the number of Streptococcus mutans NS cells adhering to glass with and without a salivary conditioning film in the presence of biosurfactant-releasing S. mitis BA and BMS (surface coverage, 1 to 4%) was significantly reduced compared with the number of S. mutans NS cells adhering to glass in the absence of S. mitis. S. mutans NS adhesion in the presence of non-biosurfactant-releasing S. mitis BA and BMS was not reduced at all. In addition, preadsorption of isolated S. mitis biosurfactants to glass drastically reduced the adhesion of S. mutans NS cells and the strength of their bonds to glass, as shown by the increased percentage of S. mutans NS cells detached by the passage of air bubbles through the flow chamber. Preadsorption of the acid-precipitated fraction inhibited S. mutans adhesion up to 80% in a dose-responsive manner. These observations indicate that S. mitis plays a protective role in the oral cavity and protects against colonization of saliva-coated surfaces by cariogenic S. mutans.

Bacterial Adhesion↗