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Oral Flora II

Oral Flora II

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Oral Flora II

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  1. Oral Flora II Karen Ross 2007

  2. Identification of Oral Microorganisms16S DNA based detection Use 2 oligo-nucleotide primers universal to ALL bacteria 16S rDNA, PCR amplification of the total saliva or plaque DNA pool, clone the PCR product and sequence. Variation allows similar species to be distinguished. Currently over 125,000 bacterial 16S sequences have been deposited in major public databases (Genbank, Ribosomal Database Project. Phylogeny -can construct a tree of evolutionary relationships In the oral cavity more than 700 bacterial species or phylotypes have been detected. At least 50% have not been cultivated yet.

  3. Schachtele et al.,2007 Oral Streptococci: Commenals and opportunistic pathogens (chapter 16) in Molecular Biology of Streptococci.

  4. Nasopharynx • S. pneumoniae • Tooth surface • mitis group • mutans group • anginosus group • Vestibular mucosa • S. vestibularis • Saliva • S. salivarius • S. mitis • S. oralis • mitis group • anginosus group • Buccal mucosa • S. mitis • mitis group • anginosus group • Tongue • S. salivarius • S. mitis • Tonsils • S. sanguis • S. mitis • S. mutans • mitis group • anginosus group • Pharynx • S. mitis • S. oralis • mitis group • anginosus group

  5. Windows of Colonization S. mitis A S. sanguinis B S. mutans C 6 12 18 24 30 36 0 Age (months)

  6. Mutans Group • S. mutans and S. sobrinus most common Virulence factors • Specific adherence to tooth surface using antigen I/II adhesin and GTF (glycosyl transferase ) • Production of extracellular polysaccharides (dextran) allows the cariogenic bacteria to stick onto the teeth and form a biofilm • acid-tolerance (aciduricity) • Able to maintain microbial growth and continue acid production at low pH values • Rapid metabolism of sugars to lactic and other organic acids • Lower the pH to below 5.5, the critical pH. Drives the dissolution of calcium phosphate (hydroxyapatite) of the tooth enamel (acidogenicity) • Accumulation of intracellular polysaccharides (carbon/energy reserve) Mitis salivarius agar levans and dextrans

  7. Streptococcus mitis • Gram+ve cocci • Binds amylase (breaks down starch in glucose) • Commensal - pathogen • Shares 99% sequence identity with S. pneumoniae • Endocarditis, toxic shock-like activity Virulence • Pneumococcal ply gene for pneumolysin and surface adhesin PsaA found in many strains • Bind platelets • Members of the mitis group are naturally competent and able to take up foreign DNA

  8. Streptococcus pneumoniae • Pneumococcus, Diplococcus pneumoniae • facultative anaerobic, gram+ bacteria, cocci in pairs, lancet-shaped, fastidious • Pneumonia, meningitis, sometimes occult bacteremia • Nasopharynx in up to 60% of the population • Major virulence factor is the capsule • Antiphagocytic • non-encapsulated organisms are avirulent • Pneumolysin, pore forming hemolysin • Stimulates production of inflammatory mediators • Activates phopholipases in endothelial cells • Toxic to pulmonary endothelial and epithelial cells • Inhibits cilial beat

  9. Endocarditis •Certain dental or medical procedures. Dental procedures that cause bleeding may allow bacteria to enter your bloodstream. Bacteria may also be a concern with procedures done elsewhere in the body, such as in the respiratory tract. •An infection or other medical condition. Bacteria may spread from an infected area, such as a skin sore. Gum disease, a sexually transmitted disease or an intestinal disorder — such as inflammatory bowel disease — also may give bacteria the opportunity to enter your bloodstream. •Catheters or needles. •Common activities. Even everyday activities such as brushing your teeth or chewing food can allow bacteria to enter your bloodstream — especially if your teeth and gums are in poor condition.

  10. Oral streptococci and infective endocarditis • Oral cavity -cause no known disease in the oral cavity except for cariogenic mutans streptococci • Blood -systemic pathogens, major cause of infective endocarditis Coagulopathies in neutropenic or immunocompromised patients • Enter the blood stream on a daily occurrence in most people, brushing ones teeth or eating an apple • S. sanguinis, S. oralis, and S. gordonii (viridans streptococci) are the most common oral streptococcal species recovered from the platelet vegetations • Attach to and colonize diseased or injured heart valves. • Virulence factors include production of dextran, glucan and other exopolysaccharide polymers which serve to encase colonized streptococci on the heart valve and resist antimicrobial attack of phagocytic cells antibodies, complement and antibodies. • Able to induce platelet aggregation. • Able to bind connective tissues

  11. Microbiota of the human mouth in health and disease

  12. Lactobacillus • Gram +ve cocobacilli alpha or non hemolytic. • L. casei, L. rhamnosus, L. acidophilus, L. oris • Ferment carbohydrates to form acids (acidogenic) • Tolerate acid (aciduric) • Major members of the normal flora of the vagina. The lactic acid product of their metabolism helps to maintain the low pH of the normal female genital tract that inhibits the growth of pathogens • Rarely cause disease • Lactobacilli in the oral cavity probably contribute to acid formation that leads to dental caries.  Lactobacillus species and a vaginal squaemous epithelial cell. CDC

  13. Actinobacillus actinomycetemcomitans • Leukotoxin -binds monocytes, neutrophils and some lymphocytes, forms pores and leakage of contents • Cytotoxins -cytolethal distending toxin (CDT)/immunosupressive factor (ISF) • LPS -bone resorption, platelet aggregation and skin necrosis • Fc-binding proteins -proteins that are associated with or released from the cell surface that bind the Fc region of Igs. Can compete with neutrophils for binding to the Fc and therefore inhibit phagocytosis. • Membranous vesicles (blebs) • Extracellular amorphous material • Fimbriae

  14. Mechanisms Adhesion Invasion of epithelial cells Colony phase variation -smooth and rough forms, rough colony variants heavily fimbriated Interference with host defense mechanisms -inhibit PMN chemotaxis, resists phagocyte killing (capsularlike material), causes release of inflammatory mediators by immune cells. Bone resorption -surface associated material (SAM) containing a heat shock protein acts directly onosteoclasts, LPS and proteolysis-sensitive factor in microvesicles. Apoptosis -leukotoxin-mediated killing through the activation of caspases, removal of acute inflammatory cells Fine et al., 1999

  15. Dentin tubule infections Pulpitis, pulp necrosis and infection of the root canal system Streptococci most commonly identified. Obligate anaerobes also in high numbers

  16. Trench mouth It is also known as ”Vincent’s stomatitis”, "Vincent's angina”, or "acute necrotizing ulcerative gingivitis” (ANUG).The common name was probably coined during World War I when many soldiers suffered from the condition. There are a number of other theories to the origin of the name. Vincent's angina was named after French physician Jean Hyacinthe Vincent (1862-1950) Fusobacterium nucleatum and the oral spirochaetes, Treponema spp. Forming a fusospirochaetal complex. If you add Clostridium perfringens you can get an oral gas gangrene equivalent.