1. What is different about mycobacteria from other types of bacteria?
    It is neither gram positive or gram negative due to staining issues.
  2. Mycobacteria are irregular-shaped __________, and are __________ bacteria.
    • Bacilli
    • Aerobic
  3. Mycobacterial membrane are rich in lipids, including __________ and __________.
    • Mycolic acid
    • Waxes
  4. Why is it necessary for prolonged treatment of mycobacterium?
    • They cause chronic disease by growing slowly
    • They become dormant in hosts for long periods of time.
  5. Describe several ways treatment of mycobacteria can be difficult.
    • Efflux pumps
    • Drugs don't penetrate the cell wall
    • They reside within host cells.
  6. In __________tuberculosis, mycobacterium tuberculosis is phagocytized by __________, and multiply intracellularly. After __________ weeks, the immune system attacks, forming __________, granulomas consisting of a central core containing bacilli surrounded by __________.
    • Primary
    • Macrophages
    • 3-4 weeks
    • Tubercles
    • Leukocytes
  7. What happens to a TB tubercle if it breaks down into necrotic lesions?
    They heal by calcification.
  8. Secondary TB occurs when tubercles expand and drain into the __________ & __________.
    • Bronchial Tubes
    • Upper Respiratory Tract
  9. What gradually worsening symptoms can one see with secondary TB?
    • Violent Coughing
    • Green and Bloody Sputum
    • Fever, Fatigue
    • Anorexia, Weight-loss
  10. First-treatment for active TB infection includes what drugs?
    Isoniazid + Rifampin + Pyrazinamide + Ethambutol
  11. Secondary TB can be treated with which drugs?
    • Isoniazid
    • Isoniazid + Rifapentine (combo)
    • Rifampin
  12. What other agents are available for the treatment of resistant TB bacteria?
    • Rifabutin
    • Rifapentine
    • Clofazimine
    • Dapsone
  13. What is isoniazid's MOA?
    It inhibits mycolic acid synthesis.
  14. How can isoniazid be both bacteristatic and bactericidal?
    It kills rapidly dividing cells.
  15. Mutations in the catalase-peroxidase enzyme can create bacterial reistance to __________.
  16. What are some common side effect's of isoniazid?
    • Rash
    • Fever
    • Jaundice
    • Peripheral Neuritis
  17. T/F: Isoniazid can have potential neurotoxicity with patient's with seizure disorders.
    True, it can cause convulsions.
  18. Isoniazid is commonly administered with __________, to prevent peripheral neuritis and CNS toxicity.
  19. __________ binds RNA polymerase and inhibits transcription initiation.
  20. T/F: Rifampin is bactericidal to gram positive bacteria only.
    False, gram negative as well.
  21. Why is resistance to rifampin common?
    Mutations in RNA polymerase
  22. Even though rifampin is generally well-tolerated, why is taking it a concern?
    It heavily induces several CYP enzymes, causing decreased levels of several drugs.
  23. Pyrazinamine inhibits __________, and is only active in __________.
    • Mycolic Acid Synthesis
    • Acidic pH
  24. Ethambutol inhibits __________, thereby inhibiting __________ in mycobacterium.
    • Arabinosyl Transferase
    • Cell Wall Synthesis
  25. Mycobacterium avium complex is an __________ infection and is commonly found in __________ patients.
    • Opportunistic
    • AIDS
  26. Prophylactic treatment of mycobacterium avium complex involves which drugs?
    Azithromycin and Clarithromycin (both macrolides)
  27. Other than macrolides, first-line treatment of mycobacterium avium consists of what other drugs?
    • Ethambutol
    • Rifabutin
  28. The two major forms of leprosy are __________ & __________.
    • Tuberculoid
    • Lepromatous
  29. Treatment of tuberculoid leprosy involves combination therapy with __________ & __________. Adding __________ is warranted for treatment of lepromatous leprosy.
    • Dapsone
    • Rifampin
    • Clofazimine
Card Set
DA mycobacterium lecture