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124 Cards in this Set
- Front
- Back
What organism is related to Agressive (early onset) periodontitis?
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-Aggregatibacter actionmycetemcomitans
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Describe Neutrophil Respiratory Burst?
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-Neutrophil metabolism is indept of O2.
-Consumes large amount of O2 when stimulated to converted to Superoxide anion and hydrogen peroxide. -Resulting in OXIDATIVE killing. |
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Defect in NADPH oxidase result in what?
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-Chronic Granulomatous Disease: inability to mount a respiratory burst.
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Describe each step that ais affect by
1. Chronic Granulomatous disease (CGD) 2. Myeloperoxidase deficient (MPOD) 3. Glycogen storage disease (GSD) |
1. CGD: NADPH oxidase
2. MPOD: MPO inhibitor (NaN3): H2O2 --> HOCl 3. GSD: O2- deficit. |
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Clinical Presenation of CGD Pt?
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-Recurrent staphylococcus skin infection (10 yr old)
-Periodontal condition deteriorated suddenly, cannot be controlled by antibiotic (38 yrs old) |
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Literature stated that pt with CGD have evidence of severe periodontal disease (T/F)
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False: Severity of diease consistent with age and oral hygiene
-50% of CGP is ass. with gingivitis. |
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Examples of Bioactive lipids?
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-Leukotriene B4
-PAF |
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Exampes of Cytokines from Neutrophil-derived Mediators?
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-IL-1, 6, 8
-TNF-Alpha -GM-CSF, G-CSF |
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Fx of Neutrophil recptors?
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-Phaygocytosis
-Modulation -Adhesion -Chemotaxis |
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Destructive roles in Neutrophil?
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-Releasing granular enzymes (elastase)
-Releasing toxic oxygen species (O2-, H2O2 -Releasing inflammatory mediators (TNF-alpha, IL-1) |
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Roles of Macrophage in Periodontal Disease in relation to LPS?
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-LPS responsive: LPS binding protein, CD14, Toll-like receptors 4 and 2.
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Example of Marcrophage Destructive mediators?
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-Synthesis of pro-inflammatory mediators (TNF-Alpha, Il-1B, IL-6, IL-8, PGE2, NO (iNOS).
-Releasing matrix metalloproteineases (MMP) |
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Example Remodeling of Macrophage in Periodontal Disease?
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-Secreting PDGF, TGF-Beta
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T-cell regulate macrophage (T/F)
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True
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What is Priming?
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-A mechanis, where by dormant neutrophils acquire a state of preactivation that enables an enhanced response to be generated onace the cells are activated or cellular signals that say "amber" but not "green".
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Example of Priming agents?
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Bacterial LPS and Cytokines
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Primed neutrophil oxidative responsiveness has been found in ___, ___, ___?
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-Acute bacterial infection, bacteremia, septicemia, inflammatory bowel disease
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Elevated systemic cytokine levels in periodontal pt have been reported and enhanced neutrophil respiratory burts has also be dependently reported (T/F)
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False: Independently reported.
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Periodontopathogens examples?
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-Porphyromonas gingivalis
-Aggregatibacter actinomycetemcomitans |
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How is Porphyromonas gingivalis strains resistant to phagocytosis? How do we deal with that problems.
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-Capsule
-Discrete proteases that cleave opsonins and chemotactic -Require specific antibodies |
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How can you kill Porphyromonas gingivalis?
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-Intracellular
-Oxygen dependent |
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Which of the follow is Porphyromas gingivalis resistant to?
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-Lactoferrin, defensins, Other oxygen-indepedent mechanisms (Proteases)
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Aggregatibacter actinomycetemcomitans can produce human neutrophils specific leukotoxins (T/F)
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True: Host antibody responses to leukotoxin and capsule
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Describe how to kill Aggregatibacter actinomycetemcomitans?
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-Easy to phagocytized
-Sensitive to Oxygen-independent killing mechanism (Lactoferrin) -Make catalase: but is sensitive to MPO system |
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Examples of PMN dysfunctions?
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-Neutropenia
-Leukocyte Adhesion Deficiencies -Chemotaxis deficiencies -Lysosomal granule dysfunctions |
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PMN evasives strategies of periopathogens?
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-Resistance to phagocytosis & opsonization
-Resistance to killing -Production of leukotoxins |
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PMN involvement in Pathology?
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-Recruitment & activation of Macrophage: cytokine directed PMN-priming (IL1B, TNFA, IL8)
-PMN produces in GCF (collagenase, B-Glu, LF, MPO) |
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What is Mouse Chamber Model?
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-Cytology
-Monokine ass. w/ PMN influx -IL8 analogue -PMN activation by chamber fluid w/o Ab or C -PMN presence w/o LTB4. |
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What type of metabolism is facultative?
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-Capable of both aerobic or anaerobic metabolism
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What is difference b/t selective and differential?
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-Differential: ie sugar fermentation
-Non-selective vs. selective |
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What percent is Cloiform bacteria (Enterics) in pyogenic oral infections?
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-6%
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Dental Unit water lines pathogen?
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-Pseudomonas: pioneer colonizer
-Peri-implant infections -Need to monitor dental unit water line and regular disinfection |
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What type of bacteria are well colonized in GI?
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-Strict Anaerobes
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Describe Coliform bacteria stain, enzyme production, structures and Selective media?
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-Stain: Gram - = endotoxin = LPS (O-antigen)
-Make exotoxins, hymolysins, proteases -Flagella (H), fimbriae, pili and capsules (K) -Selective media: MacConkey's Agar. |
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Classic stimulant for inflammatory response?
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-Gram - = endotoxin = LPS (o antigen)
-Step1 : LPS + LPS binding protein --> CD14 on Monocytes, -Step2: LPS + CD14 --> TLR 4 on Monocytes -Step3: Activation of NFB--> Inflammatory mediator |
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Growth in bile salts and dyes inhibit what?
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-Gram +s
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What are the serotypes of E. Coli?
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-O antigen CHO side chain of LPS (serogroup)
-H antigen (protein-flagellin) of flagella (serotype) -K antigen of capsule (CHO) -Virulence ass |
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How does virotypes occur?
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-Typing based on virulence traits
-Certain serotypes more ass. |
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Virotypes of E. Coli
-ETEC -EAggEC -EPEC -EHEC -EIEC |
-ETEC (toxic): attach but not invade
-EAggEC: similar to ETEC -EPEC (pathogenic): provoke inflammation -EHEC (hemorrhagic): kidney failure), shiga toxin -EIEC (Invasive): invade colonic cells but don't produce Shiga-toxin |
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Uropathogenic E. coli?
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-Community acquired: Uropathogenic strains (>80%), Lkebsiella, Proteus, start colonizing in colon, Urethra & Bladder --> Kidneys
-Hospital Acquired: 50% of pt w/ indwelling urinary catheter for > 5 days (septicemia) -Hematogenous urinary tract infection. |
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What is Hematogenous urinary tract infection gram stain?
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-Almost always Gram +, Descending infections
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Major cytokines released during septic shock?
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-IL1A + B
-TNF -IL6 -IL8 -Interferon-Gamma. |
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Respiratory Infection
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Respiratory Infection
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Aerotolerant Respiratory Pathogens in oral-Facial infections?
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-Streptococcus pyogenes
-Staphyloccus aureus -Klebsiella pneumonia |
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Describe Streptoccocus Pyogenes (stain, sugar, hemolysis, sensitivity)
(+, B, CN, A, B) Plus BoW Can Never Achieve B grade |
-Gram + cocci in chains
-Beta Hymolytic small white colonies -Catalase negative (no bubbles w/ H2O2) -Serogroup A-Lancefield typing -Sensitive to Bacitracin (Group A disk) |
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Staphlyoccous aureus (stain, sugar, hemolysis, sensitivity)
(+, B, C, SM, P) Put Billy Can SwiM Permenantly. |
-Gram + cocci in clusters
-B-hemolytic-yellow large colonies -Catalase postive (bubbles w/ H2O2) -Growth in salt and mannitol -Resistant to penicillin |
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Klebsiella pneumonia (stain, sugar, hemolysis, sensitivity)
(-, L, C, in M, BM) Never lack Capsule in My Blue Meth) |
-Gram - rod
-Ferment lactose -Capsule production -Growth in bile salts MacConkey's or Eosin Methylene Blue (EMB) |
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Located of S. aureus vs S. pyogenes
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-S. aureus: resident microfloa of nose, vagina, colon
-S. pyogenes: carries, upper respiratory tract |
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Disease caused by both S. aureus and S. pyogenes
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-Impetigo
-Speticemia |
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Diseased caused by S. aureus and not by S. pyogenes?
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-S. aureus: food borne disease, soft tissue infections, Pnuemonia, Osteomyelitis
-S. pyogenes: Pharyngitis (rheumatic fever; kidney failure), Boils, skin abscesses, TSLS, Scarlet fever |
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Describe S. pyogenes Pharyngitis?
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-Sudden onset, swollen tonsils, purulent exudate of tonsils, low-grade fever, pain mild to severe
-May cause severe pneumonia -Rheumatic fever rate > 2% if not treated. |
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Invasive Group A Streptococci?
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-Symptoms occur w/in 1-2 days
-Acute Respiratory: pain in chest, high fever, BP drop, Scarlet fever -Wound Infection: pain, high gever, BP drop, Necrotizing lesion |
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TX of Invasive Group A Streptococci?
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-Tx broken skin w/ betadyne or other good antiseptic and cover
-Tx with penicllin or Augmentin -Early tx is impt. |
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S. pyogenes is ALWAYS susceptible to penicillin (T/F)
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True
-Heart ass: penicillin or other regimen required to prevent rheumatic fever. |
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Smallest free living bacteria?
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-Mycoplasma pneumonia
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Where and who does Mycoplasma pneumonia infect?
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-Respiratory mucosa: P1 adhesion binds to base of cilia on epithelia cells.
-Droplet transmission (common in children) -Slow onset, clear to cloudy white discharge -Last 2-5 wks -Pas middle age or impaired health |
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Mycoplasma Respiratory INfections?
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-Upper respiratory (URI): pharyngitis, rhinitis, sinusitis, Eustachian tube/middle ear infections, moves from one side to other.
-Lower respiratory (LRI): Brochitis, pneumonia (Atypical or walking pneumonia) |
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Mycoplasma susceptiblity?
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-No cell wall for target (Resistant to Penicillin, cephalosporin, vancomycin)
-Drugs prevent protein synthesis -Erythromycin 500 units QID -Oxycycline (Vibramycin) 100 mg. |
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Factors that affect pt who get Legionella pneumophila?
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-Fastidious and hard to stain
-Factors: men over 55 years, smoking, alcohol abuser OR -Emphysema; chronic bronchitis; diabetes; cancer/chemotherapy -Source: water aerosols-dentul unit water lines -Not transmissible. |
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Legionallosis URI?
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-Pontiac fever
-Pharyngeal/rhinitis -High infectivity rate -Short lived, 2-5 days |
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Legionellosis LRI?
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-Sudden onset
-Chills/fever -Lung congestion -Erythromycin or tetracycline |
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What is Cystic Fibrosis?
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-Defective chloride transport (cystic fibrosis transmembrane conduct regulator (CFTR) gene)
-Leads to reduced aqueous phase w/ increase mucin-defective beating of cilia and reduced mechanical clearance |
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About half of infectious colds are believed to be caused by rhinoviruses (piconaviridae). (T/F)
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True
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Common URI cold viruses
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-Picorna-rhinovirus
-Coronavirus -Respiratory syncytial virus |
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What affect does Rhino viral agents have?
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-Damage mucosal cells and membranes
-Provoke increased vascular permeability (kinins, histamine, iNOS) -Lipid breakdown -Fever/pain (PGE2, pyrogen) -Edema (pus infection) |
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Live virus can proliferate cause what?
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-Acute febriel/pain response
-Slough ciliated epithelial cells -Edema may seal respiratory passages -Edema or 2nd bacterial infection can kill in 3-6 days. |
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Viral infection is halted by ___ secreted by mucosa, usually in ___ days
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-Interferon in 2-4 days
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Immunity (sIgA) usually responds ___ weeks.
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-2
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Viral relapse and recovery may occur before antibody response (T/F)
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True
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Recommended tx for Mucosal damage (coughing)?
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-Topical or systemic vasoconstrictors to relieve nasal congestion, analgesics to treat headache.
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Most vaccines stimulate IgA (T/F)
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False: IgG
-Nasal flu vaccine stimulates SIgA response through common mucosal immune system |
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If untreated, rhinitis can lead to what?
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-Sinusitis, otitis media, bronchitis, pneumonia, or late-occuring problems such as nasal polyps and brochiectasis.
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Sinus infection occurs when?
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-Infection w/o adequate drainage = growth of resient bacteria
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Bacterial agents of Sinus RI?
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-Mycoplasma
-Hemophilus influenza -S. pyogenes -Branhamella catarrhalis (Neisseria) -Streptococcus pneumonia |
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Half of global population is infected wiht Mycobacterium tuberculosis (T/F)
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False: 1/3
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What is the vaccine for TB?
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-Calmette-Guerin (BCG)
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Fungal infections of Lower respiratory tracts?
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-Inhale spores or yeast
-Immunocompromised -Blastomycosis, coccidiomycosis, cryptococcosis, histoplasmosis |
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Pneumonias due to Pneumocystis carinii are particularly common in AIDS (T/F)
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True
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Cause of non-seasonal allergies
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-Chronic or recurring symptoms of nasal obstruction w/ or w/o discharge
-Food allergens -Sensitivity test helpful |
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What is SARS
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-Severe Acute Respiratory Syndrome
-Coronavirus -Development of antibodies (>21 days) |
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Symptom?
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-Mild: Asymptomatic
-Moderate: fever, cough, shortness of breath -Severe: fever, cough, shortness of breath, hypoxia, radiographic PNEUMONIA, Respiratory distress syndrome. |
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END OF ENTERIC BACTERIA
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END OF ENTERIC BACTERIA
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Methods of ID of bacteria?
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-Culture: isolation, ID and determination of antibiotic sensitivities
-DNA-DNA hybridization -PCR -Serological ID |
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What Capnophilic and Microaerophilic?
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-Capnophilic: candle jar and or CO2 incubator
-Microaerophilic: aerobic bacteria that find atmospheric O2 toxic. |
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Natural habitat of most oral bacteria?
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-Structural multi-species communit.
-Bacteria embedded in matrix w/ water channels -Attachment - growth - ecological - maturation |
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Describe Sub-g tooth surfaces
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-Low O2 tension = Good G- anaerobes
-Major site of interaction of bacteria/host tissues -Species mix varies b/t each side |
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Basic biofilms properties
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-Cooperating communities of various types of micro-organisms
-Antagonism -Arrange in microcolonies -Surrounded by protective matrix -W/in microcolonies are diff environment -Microorganism have primitive communication sys. -Resistant to antibiotics, antimicrobials and host responses |
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-Biofilms behave as a community (T/F)
-Assemblage of microorganisms: self-organize (T/F) -Respond to environmental changes as a individual (T/F) |
-True
-True -False: unit |
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Who does microcolonines communicate with as scouts?
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-Planktonic
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What Quorum sensing?
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-Tells bacteria when to grow and when its time to go.
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What is the goals of deattaching bacteria at the surface of mature biofilms?
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-Bacteria become planktonic and find a new ome
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Saliva provide a transport medium for planktonic oral bacteria to travel and grow (T/F)
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False: For travel only not growth.
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Ecological succession
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-3rd colonizers: (Gram -): Porphyromonas gingivalis
-2nd colonizers: (Gram -): Bridge species, F. nucleatum bind to other bacteria -1st (Gram +): Streptococcus bind pellicle proteins from saliva. |
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List microbial complex in green cluster?
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-C. gingivalis, E. corrodens, S, sputigena, C. orchracea, C. concisus, A. actinomycetemcomitans serotype A
|
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Host Resistance Properties?
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-Innate immune defense factors
-Antibodies -Phagocytic cells -Epithelial integrity -Indigenous host compatible microfloa -Nutritional deprivation |
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Host Suceptibility to Traits?
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-PMN dysfunctions (overt or subtle)
-Opsonin dysfunctions -Hyperresponsive inflammatory response -Anatomical -Environmental (oral hygiene, diet) -Tissue repair/regeneration |
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Innate defense resistance of bacteria.
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-Serum
-PMN -Oxygen tolerance -Inactivation by proteases |
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Attachment of bacteria?
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-Fimbriae
-Capsule -Hydrophobicity -Lectin/Protein receptors -Unmask receptors by proteases |
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Immune surveillance evasion?
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-Ig/Opsonin proteases
-Pleomorphism -Immunomodulation -Tissue invasion |
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Criteria for determing the etiologic agents of destructive periodontal disease?
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-Animal Models
-Host response -Association -Virulence factors -Elimination |
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Applied criterion for Porphyromonas gingivalis
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-Ass: elevated periodontal lesions.
-Elimi: Eliminate results in successful therapy -Host: Elevated serum Ab in periodontitis -Virulence: Specific proteases, endotoxin, capsule, fimbriae -Animal: mice, rats, monkeys, dogs |
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Describe Porphyromonas gingivalis?
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-Virulent strains are resistants to phagocytosis: capsule, discrete proteases
-Killing: intracellular, O2 dependent -Resistant: Lactoferrin, defensins, O2 indept. mechanisms |
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Virulence factors of P. gingivalis?
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-LPS, proteases, fimbriae, hemagglutinating factors, polysaccharides capsule, collagenase, vessicles.
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Describe LPS of P. gingivalis?
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-A potent monocyte stimulation and neutrophil priming agent TLR2
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Describe Proteases of P. gingivalis?
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-Arginine gingipain (RGP) and lysine gingipain (KGP)= inflammation
-Responsible for resistance to PMN phagocytosis and non-oxygen dependent killing mechanism |
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Aggregatibacter (Actinobacillus) Actinomycetemcomitans criterions?
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-Ass: can be almost pure culture from aggressive lesion
-Elimn: elimination results in successful therapy -Host: Prcipitating antibodies to carb. Leukotoxin neutralizing Ab. -Virulence: Leukotoxin, invasion in cell culture -Animal: Induction of disease in gnotobiotic rats. |
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Ab neutralization of virulence properties?
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-Agglutination-mech. clearance
-Masking ligand-receptor interaction (inhibit attachment) -Opsonins -Neutralization of proteases -Leukotoxin neutralization -Disrupt of biofilm. |
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Bacteria in aggressive periodontitis?
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-All species (esp. red complex) are present in periodontitis found in aggressive periodontitis.
-A. actinomycetemcomitans in early onset agg. periodontitis |
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Adult flora in children, suspect what?
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-Neutropenia, LAD
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Identify 6 bacterias associated WITH FAILING IMPANTS?
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P. gingivalis
Peptostreptococcus micros Fusobacterium sp Pseudomonas sp. Enterobacter E. coli |
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Identify the main bacteria associated with periaplical abscesses?
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Oral streptococci
Enterococcus sp S. aureus Psorphyromonas sp. P. endodontalis Prevotella sp Fusobacterium sp. Spirochetes |
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Identify the bacteria found in BOTH periapical abscesses and failing implants?
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Fusobacterium sp.
Porphyromonas species |
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Which bacterias associated with periapical abscesses are consider BACTEROIDES?
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Porphyromonas sp.
P. endodontalis Prevotella sp |
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Most UNC pt. that comes in with enodontic infections but has NO PROGRESSIVE SWELLING/FEVER are mainly treated with what?
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Ca(OH)2, without antibiotics even if they release suppurative exudate into the canal.
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If UNC pt. comes in with FEVER/PROGRESSIVE SWELLING, what should you refer to the pt.
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Orofacial surgery
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What is the most common endodontic case found in private dentist?
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Persistent or mildly progressive periapical infection
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What is the least common endodontic case found in private dentistry?
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Swelling in the face
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Dispersed bacteria can can cause infection by traveling thru ________ or ________.
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Lymphatics
Capillaries |
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Identify the bacteria with the highest percentage found in pyogenic oral infections at the school of UNC?
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Oral streptococci with 61%
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What are 4 factors related to POSTOPERATIVE INFECTION?
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size of bacterial inoculum
extent and time of surgery presence of foreign body state of host |
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What are 3 situation in which the STATE OF THE HOST could cause postoperative infection?
|
Compromised resistance
AIDS Gingivitis meaning loss of resistant against plaque bacteria CD4 T helper lymphocytes counts are less thatn 200/mm3 |
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What are 7 physical conditions that contributes to progressive oral infections?
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1. Protected reservoirs
2. Particles of calculus 3. Untreated canal with necrotic pulp 4. Fragment of root tip 5. Cracked tooth 6. PMNs cannot surround bacteria 7. Co-infection with synergistic bacteria |
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What are things you can do to AVOID POST TREATMENT INFECTIONS?
|
1. Reduce surgical trauma
2. Reduce length of surgeries 3. Reduced debris from plaque and calculus 4. Use excellent asepsis 5. Fresh sterile saline for irrigation 6. Have pt. rinse mouth with topical disinfectant 7. Neve rblow air into cut tissue 8. Don't pull long sutures across pt. hair or clothing 9. Wipe mucosa before injection |
|
Pt. are often refer to the maxillofacial surgery when there are presence of what?
|
Chills/Fever in past 24h
Progressive swelling Worsening pain, malaise |