Micro T3 Neisseria

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ashley.shaunak
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184516
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Micro T3 Neisseria
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2012-11-19 18:22:14
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Micro T3 Neisseria
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Micro T3 Neisseria
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  1. Clinical diseases caused by Neisseria Gonorrhoeae?
    Gonorrhea and Gonococcemia
  2. Neisseria Meningitidis causes what diseases?
    Meningitis and Meningococcemia
  3. When do species of Neisseria besides Gonorrhoeae and Meningitis cause disease?
    Only if immunocompromised
  4. Prevalence/Mortality of Neisseria Gonorrhea and Meningitidis
    • N. gonorrhoeae—high prevalence; low mortality
    • N. meningitidis—low prevalence;high mortality (except in belt in Agrica)
  5. Is Neisseria Gram positive or gram negative
    What is it's physical appearance?
    Is is oxidase positive?
    Is it motile?
    • Neisseria is GN
    • is it a diploccus. Can also form chains.
    • It is Oxidase POSITIVE and Aerobic
    • It is non-motile
  6. Why did Gonorrhea increase in the 1940s and in the 1980s?
    • 1940s-WWII
    • 1980s-Improved Contraceptives=more sex
  7. What is the only “state” that has more Gonorrhea than Mississippi?
    District of Columbia
  8. What are the symptoms of Neisseria meningitidis?
    Earache, headache, neck pain, fever, recent vomiting, confusion, inability to follow commands, photophobia, irritability
  9. What are the signs of N. meningitidis?
    • Cloudy fluid in lumbar puncture with over 6,000 white cells
    • GN Diplococci
    • Stiff neck on physical exam
  10. How long does it take for symptoms of N. meningitidis to show up?
    • 1-4 days
    • If severe, 1 day
  11. Is N. meningitidis oxidase/catalase positive/negative?
    Oxidase and catalase positive
  12. What kind of agar does N. meningitidis grow on?
    Chocolate blood agar (slightly fastidious) or Thayer Martin agar
  13. What are the virulence factors of Neisseria meningitidis?
    • Polysaccharide capsule
    • Serogroups A, B, C, Y, and W-135 are in 90% of infections
    • LOS(shorter side chain than LPS)
    • Endotoxin
    • Pili
    • Por and Opa proteins
    • Reduction-modifiable protein
    • Membrane blebs
    • IgA1 protease
    • Iron acquiring proteins
  14. How do the pili of N. meningitidis help with virulence?
    • Attach to epithelial cells
    • Resistance to killing by neutrophils
    • Phase variation/antigenic variation in pilin proteins
    • Induce antigens that lead to ruffling of membrane and allows access of organism into the cell
    • (it’s hard for the host to recognize organism when it is inside the cell)
  15. How does the LOS of N. meningitidis help w/virulence?
    The lipid A (endotoxin moiety) stimulates inflammatory response and release of TNF-a
  16. How do the PorB proteins of N. meningitidis work?
    • They are outer membrane proteins that form pores
    • They protect the bacteria from the host’s inflammatory response
    • They facilitate bacterial invasion into epithelial cells
  17. How do the Opa proteins of N. meningitidis work?
    • They are Outer Membrane Proteins
    • They bind to epithelial cells
  18. What is the role of Reduction-modifiable protein (RMP) in N. meningitidis virulence?
    • Outer membrane protein
    • IgG and IgA1 antibodies directed against these inferfere with the bactericidal action of the antibodies directed against LOS (co-interference, which is good for survival of bacteria)
  19. What iron acquisition proteins are included in the N. meningitidis?
    Transferrin, lactoferrin, and hemoglobin binding proteins
  20. How do membrane blebs help with N. meningitidis virulence?
    • They may enhance endotoxin-mediated toxicity
    • They protect bacterial cells from antibodies (like a decoy)
  21. How does the IgA1 protease help with virulence?
    It degrades mucosal IgA
  22. Characterisitcs of Meningitis (disease)?
    • Disease begins abruptly, often with fever/headache/stiff neck
    • May see non specific signs in young children
    • Mortality is 10% w/therapy, almost 100% without therapy
    • Sequelae include hearing deficits, learning deficits, and arthritis
  23. What are the charactersistics of Meningococcemia (disease)?
    • Septicemia (w or w/o meningitis)
    • Multiorgan involvement
    • Petechial skin lesions that make larger hemorrhagic leisions
    • DIC and shock
  24. What is serum resistance for N. meningitidis?
    • The organism can survive in serum by inactivating complement
    • --blocks the formation of the C5b-9 complex Membrane Attack Complex) by binding factor H and C5b
  25. What are the components of the Meningitis Vaccine? When is it given?
    • 4 serogroups (A, C, Y, and W-135)—Not B serogroup due to too many side effects
    • Conjugate Vaccine (MCV4)
    • Recommended for preadolescence with a booster before college or 1st shot before college
  26. Treatment of N. meningitidis/Prevention
    • Penicillin
    • Cephalosporins
    • MCV4 vaccine to prevent at 11-12 years old and boost at college age (close quarters=outbreaks)
  27. Other diseases caused by N. meningitidis
    • Pharyngitis
    • Pneumonia
    • Urethritis
  28. Epidemiology of N. meningitidiis
    • Humans are only natural host
    • Aerolized spread
    • Highest incidence in 16-21 year olds****
    • Occurs most commonly in dry, cold months
  29. Where do N. sicca and N. mucosa live? What do you treat them with? What diseases do they cause?
    • Oropharynx (commensals)
    • Susceptible to penicillin
    • Meningitis, osteomyleitis, otitis media, sinustitis
  30. Morphology/Gram stain/Classification of Eikenella corrodens
    • GN non spore forming rod
    • Facultative anaerobe
  31. Where does eikenella corrodens normally live? What injury is it associated with? What do you treat with
    • Human oropharynx
    • Human bite wounds or fistfight injuries
    • Susceptible to penicillin, ampicillin, cephalosporins, tetracycline, and fluroquinolones
  32. What does eikenella corrodens look like when it goes?
    Indents/corrodes the agar when it grows
  33. What are the HACEK diseases? What do they cause?
    • Hemophilus
    • Actinobacillus
    • Cardiobacterium
    • Eikenella
    • Kingella
    • They cause subacute endocarditis
  34. What is the gram stain of Kingella kingae? Where does it live? What do you treat with?
    • GN coccobacillus
    • Lives in human oropharynx
    • Treat with penicillin, tetracycline, erythromycin, fluoroquinolones, and aminoglycosides
  35. What does Kingella kingae cause?
    Septic arthritis
  36. What is the gram stain Moraxella catarrhalis? Is it aerobic? Is it oxidase positive?Where does it live?
    • GN diplococcic
    • Aerobic and oxidase positive
    • Lives in human respiratory tract (commensal). Most often seen in children or adults with COPD.
  37. What diseases are associated with Moraxella catarrhalis?
    • 3rd leading cause of otitis media in young children
    • Bronchitis and bronchopneumonia in elderly patients with COPD (Major cause of COPD exacerbations)
  38. What is a virulence factor that Moraxella catarrhalis has that makes it harder to treat?
    Has a beta lactamase, so it indirectly protects other pathogens from penicillin and is harder to treat
  39. What are other virulence factors of M. catarrhalis?
    • Adhesions
    • Inactivates complement
    • Biofilm important in otitis media

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