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Pioneer Colonizers in the Retrievable Enamel Chip Model
- Streptococcus oralis
- Streptococcus mitis
- Streptococcus salivarius
- Actinomyces spp.
- Veillonella spp.
- Neisseria spp.
- All G(+), no spores
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Streptococcus mutans
- transmitted by contact -> Colonization -> Acid production -> Demineralization -> Cavitation
- Adherence to tooth surface
- Production of extracellular polysaccharide (protection)
- Acidogenesis and Aciduricity (competency)
- Significant in causing caries
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Antigen I/II
- Binding to salivary pellicle
- Autoaggregation
- Coaggregation
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GTF
- Glucosyltransferase
- Made by Streptococcus, Lactococcus and Lactobacillus
- Transform sucrose into glucans and fructose (converted to lactic acid)
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autoaggregation of S. mutans is mediated by
GBP, between the cell and glucans, forming a robust biofilm
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Saliva prevents caries
- Mechanical washing - flow rate, Xerostomia, circadian rhythm
- Buffering - sugary diet; Stephan cu
- Antibacterial activity
- Aggregation of bacteria
- Remineralization of enamel
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Prevention of Dental Caries
- Interfere with transmission
- Eliminate S. mutans from the oral cavity
- Increase acid resistance of enamel
- Control carbohydrate composition of diet
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Interfere with transmission
- Vaccines
- Enzymes (mutanase and dextranase)
- Strain replacement therapy
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Eliminate S. mutans from the oral cavity
- Mechanical removal of plaque
- Biocides (chlorhexidine, SDS, CPC, antibiotics, bacteriocins)
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Increase acid resistance of eanmel
- Fluoride
- Pit and fissure sealants
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Control carbohydrate composition of diet
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Staphylococcus are in ________, while Streptococcus are in _________.
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Staphylococcus
- G + cocci
- 0.5-1.5 um
- Nonmotile, no flagella, etc
- Facultative anaerobic
- Can grow in high salt (10% NaCl)
- 18-40 C
- Part of the normal flora (nasal, skin) - S. aureus and S. epidermidis, do not cause disease until they get into blood
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S. aureus has ____ colonies and S. epidermidis has ____ colonies.
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S. epidermidis causes
- device infections
- bacteremia
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S. aureus causes
- many more infections, including wound and burn infections
- high resistance
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Catalase test on Staph vs Strep
- Catalase catalyze H2O2 to H2O and O2
- Staph has catalase, after adding H2O2, foamy.
- Strep doesn't have catalase, no much effect.
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Capsular polysaccharide Protects against phagocytosis
- S. aureus has 11 capsule serotypes.
- Serotype 5 and 7 are associated with infection.
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Slime Layer
Mediates adhesion to epithelial cells and biofilm formation.
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Peptidoglycan
- Half of the cell wall weight is peptidoglycan.
- In MRSA mecA codes for PBP2 that does not bind penicillin.
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MSCRAMMs
Microbial surface components recognizing adhesive matrix molecules
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Teichoic acid
structure that goes through G+ bacteria that allows them to stick to the organism as well
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Protein A
- Coats surface of S. aureus
- very high affinity for the Fc receptor of IgG (IgG tags the cell in a wrong way)
- prevent opsonization and phagocytosis.
- inhibit antibody mediated clearance.
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surface protein on S. aureus - Coagulase
- Cell free coagulase.
- Converts fibrinogen to insoluble fibrin, which causes
- clumping and aggregation.
- Collagenase - can cause the formation of a protective fibrin layer around the cell.
- S. aureus is coagulase positive; S. epidermidis is coagulase negative.
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Other Extracellular enzymes
Fibrinolysin or Staphylokinase, Hyaluronidase, Lipase, Deoxyribonuclease, Fatty acid modifying enzyme (FAME)
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S. aureus Toxins
- α-toxin (α-hemolysin) - Forms pores in cell membranes and causes tissue damage.
- β-toxin - Hydrolysis of membranes.
- δ-toxin - Nonspecific membrane toxin.
- γ-toxin and Panton-Valentine (PV) leukocidin- Lyse neutrophils and macrophages.
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Exotoxins
- Exfoliating toxin A and B - Serine protease, Staphylococcal scalded skin syndrome (SSSS)
- Enterotoxins (A-E, G-I) - food poisoning, resistant to high temp, and gastric enzymes.
- TSST-1 - toxic shock syndrome toxin - 1, Superantigens, bind to macrophages and interact with T-Cells and releases cytokines- shock and high fever and organ failure.
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HA-MRSA
- • Hospital acquired.
- • Typically found in immunodeficient patients.
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CA-MRSA
- • Community acquired.
- • Typically found in healthy individuals.
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Staphylococcus epidermidis
- most common bacteria on skin.
- Found on everyone.
- Opportunistic pathogen.
- Coagulase negative Staphylococci
- medical devices colonizing
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poly-N-acetylglucosamine
- Attachment to biomaterials. Biofilm formation.
- Protection from antimicrobial killing and phagocytosis.
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Streptococcus pyogenes - group __ streptococci; causes
- Group A
- Puerperal fever (childbed fever)
- Pharyngitis (Strep throat)
- Scarlet fever
- Rheumatic fever
- Bacteremia
- Cellulitis (skin infection)
- Acute necrotizing fasciitis (flesh-eating bacteria)
- Toxic shock syndrome
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S. pyogenes virulence factors
- Avoiding opsonization and phagocytosis
- Surface attachment.
- Cell invasion.
- Toxins.
- Enzymes.
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S. pyogenes capsule
hyaluronic acid capsule weak immunogen
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M protein
- binds to host proteins to avoid detection
- Protects against phagocytosis
- Mediates attachment to keratinocytes
- Autoaggregation
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Toxins
- S. pyogenes exotoxin (Spe)- superantigen, releases cytokine release, cause toxic shock-like syndrome (TSLS), rash and necrotizing fasciitis (flesh-eating).
- Streptolysin S - cell-bound hemolysin, which is responsible for lyses of blood cell.
- Streptolysin O - also an hemolysin.
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Enzymes
- Streptokinase A and B - cleave plasminogen and lyse blood clots.
- DNases A-D- reduce DNA in pus, which can aid in bacteria spread.
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Streptococcus agalactiae - Group ?
B
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Streptococcus agalactiae causes
- Infection in newborn - Group B streptococci colonize the vaginal and gastrointestinal tracts in 15%-45% of healthy women; protected by ointment.
- underlying abnormalities
- • Bacteremia
- • Pneumonia
- • Wound infection
- • Urinary tract infection
- • Skin infection
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S. agalactiae - virulent factors
- polysaccharide capsule reduces phagocytosis
- Toxin- β-hemolysin
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Streptococcus pneumoniae
- G +
- Dilococci- in pairs
- Encapsulated - smooth colony vs rough colony
- grow only on enriched media with blood
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S. pneumoniae - virulent factors
- 90 capsule serotypes
- Surface protein adhesions.
- mediate cytokine production, inflammation - fever, and tissue damage.
- Phosphocholine on the cell well can mediate cell and tissue invasion, allowing protection from opsonization and phagocytosis.
- Choline-binding Proteins
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