Polymerase chain reaction detection of Lactobacillus acidophilus in human oral cavity and fecal samples after 2-week consumption of yoghurt.

OBJECTIVE: To investigate whether short-term daily consumption of yoghurt leads to colonization by Lactobacillus acidophilus in a group of human subjects who were initially totally devoid of L. acidophilus in their oral cavities. MATERIAL AND METHODS: Twenty-three volunteers consumed yogurt containing L. acidophilus during a 14-day trial stage. Oral and fecal samples were collected at the clearance stage and at the post-yoghurt intake stage until L. acidophilus was found. Standard polymerase chain reaction methods using specific primers were adopted for the detection and identification of L. acidophilus. RESULTS: The isolation frequency decreased rapidly 72 h after stopping intake of yoghurt. After 1 week, L. acidophilus was absent in all oral samples. Non-significant differences were found between the survival rates of L. acidophilus in samples of saliva, plaque, tongue surface, and buccal mucosa. L. acidophilus was also found to remain in the gastrointestinal tract for longer than in the oral cavity. CONCLUSION: Allochthonous L. acidophilus is not likely to permanently colonize the oral cavity and intestine.

Competition between yogurt probiotics and periodontal pathogens in vitro.

OBJECTIVE: To investigate the competition between probiotics in bio-yogurt and periodontal pathogens in vitro. MATERIAL AND METHODS: The antimicrobial activity of bio-yogurt was studied by agar diffusion assays, using eight species of putative periodontal pathogens and a 'protective bacteria' as indicator strains. Four probiotic bacterial species (Lactobacillus bulgaricus, Streptococcus thermophilus, Lactobacillus acidophilus, and Bifidobacterium) were isolated from yogurt and used to rate the competitive exclusion between probiotics and periodontal pathogens. RESULTS: Fresh yogurt inhibited all the periodontal pathogens included in this work, showing inhibition zones ranging from 9.3 (standard deviation 0.6) mm to 17.3 (standard deviation 1.7) mm, whereas heat-treated yogurt showed lower antimicrobial activity. In addition, neither fresh yogurt nor heat-treated yogurt inhibited the 'protective bacteria', Streptococcus sanguinis. The competition between yogurt probiotics and periodontal pathogens depended on the sequence of inoculation. When probiotics were inoculated first, Bifidobacterium inhibited Porphyromonas gingivalis, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, Porphyromonas circumdentaria, and Prevotella nigrescens; L. acidophilus inhibited P. gingivalis, A. actinomycetemcomitans, P. circumdentaria, P. nigrescens, and Peptostreptococcus anaerobius; L. bulgaricus inhibited P. gingivalis, A. actinomycetemcomitans, and P. nigrescens; and S. thermophilus inhibited P. gingivalis, F. nucleatum, and P. nigrescens. However, their antimicrobial properties were reduced when both species (probiotics and periodontal pathogens) were inoculated simultaneously. When periodontal pathogens were inoculated first, Prevotella intermedia inhibited Bifidobacterium and S. thermophilus. CONCLUSIONS: The results demonstrated that bio-yogurt and the probiotics that it contains are capable of inhibiting specific periodontal pathogens but have no effect on the periodontal protective bacteria.

Defect of cell wall construction may shield oral bacteria's survival in bloodstream and cause infective endocarditis.

Infective endocarditis (IE) is a rare but life-threatening infection. Bacteremia with organisms known to cause IE occurs commonly in association with invasive dental origin. Despite daily oral activities as well as professional dental treatments inducing bacteremia and the dental bacteremia as a risk factor of IE, the details of dental bacteria in the pathogenesis of IE are far from elucidation to date. How do a few microorganisms survive host defenses or escape from antibiotic attacking to seed target organs and cause distant infections? Why are Gram-positive bacteria more frequently detected than Gram-negative bacteria in IE? Cell wall-deficient bacteria (CWDB) were traditionally defined as bacteria with altered morphology and consistent with damaged or absent cell wall structures identified by EM. A number of case reports and laboratory studies suggest that CWDB may be found in the peripheral blood of patients with IE, and may also be demonstrated in vegetations on the valves of patients with IE. CWDB, in vitro, are resistant to antibiotics that act on cell wall biosynthesis. Recent studies indicate that the Streptococcus mutans (S. mutans) strains, the major cariogenic bacterium, isolated from the infected valve were deficient in some wall-associated proteins which are main cariogenic virulence of S. mutans, and the deficient stains exhibited less susceptible to antibiotics that act on cell wall biosynthesis. Further, the cloned deficient mutans were less susceptible to phagocytosis by human polymorphonuclear leukocytes but to possess higher platelet aggregation properties than their parent strains. As outlined above, we hypothesize that defect of cell wall construction may shield oral bacteria's survival in bloodstream and cause IE.