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233 FINAL > Antimicrobial 3: Antimycobacterials > Flashcards

Antimicrobial 3: Antimycobacterials Flashcards

1
Q

Name 2 main mycobacterial infections in humans:

A

tuberculosis (TB):
chronic infections caused by Mycobacterium tuberculosis

leprosy
chronic infections caused by Mycobacterium leprae

Mycobacterium are capable of surviving inside
macrophages after phagocytosis

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2
Q

tuberculosis (TB)

Characteristics

A

• TB usually affects the lungs and is associated with
chronic cough with blood-containing sputum

• Tuberculosis results almost exclusively through
inhalation of airborne particles that contain M.
tuberculosis

• Dispersed/spread through forced respiratory
maneuvers by those with active TB (e.g. coughing,
singing)

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3
Q

tuberculosis (TB)

Symptoms

A

Active pulmonary tuberculosis
symptoms:

  • Most common symptom: Cough (becomes more
    productive as disease progresses)
  • May have no symptoms aside from ”not feeling well”,
    anorexia, fatigue, weight loss
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4
Q

Leprosy

Characteristics

A

• Leprosy mainly affects the skin and peripheral nerves

• Leprosy is an ancient disease that causes a chronic
disfiguring illness with long latency (2 types:
paucibacillary or multibacillary)
- Paucibacillary: T cell response dominated by interferon gamma - enhances macrophage’s ability To eliminate mycobacteria- treatment not as long
- Multibacillary: T cell response dominated by IL-4 response which can interfere with IF-gamma, macrophages fail to eradicate as good
• Spread person to person through nasal droplets and
secretions

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5
Q

Leprosy

Symptoms

A

Symptoms include non-pruritic rash, numbness and weakness of areas controlled by affected nerves

Not highly contagious - believed to be contagious due to appearance

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6
Q

Leprosy

Name 2 types of leprosy:

A
  1. tuberculoid leprosy
  2. lepromatous leprosy

Depending on type, different presentation of skin lesions, skin macules, papules, plaques

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7
Q

TB

Pharmacotherapy

A
  • Initial phase of treatment includes isoniazid, rifampicin and pyrazinamide (and possibly ethambutol) for 2- months
  • Continuation phase includes treatment with isoniazid and rifampicin for 4-months

• Combination therapy is used to avoid the development of drug resistance

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8
Q

Leprosy

Pharmacotherapy

A
  • Tuberculoid leprosy treated with dapsone and
    rifampicin for 6-months
  • Lepromatous leprosy treated with dapsone,
    rifampicin, and clofazimine for 2-years

• Combination therapy is used to avoid the
development of drug resistance

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9
Q

Mycobacterial Cell Wall

Characteristics

A

• The mycobacterial cell wall is composed of a
peptidoglycan (PG) - arabinogalactan (AG) - mycolic
acid (MA) structure
- classified as G+ with peptidoglycan

• Mycobacteria, similar to gram negative bacteria, do
NOT retain the crystal violet stain. However, they are
classified as acid-fast gram positive bacteria due to
their lack of an outer cell membrane

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10
Q

tuberculosis (TB)

First-line Agents

Combination therapy is usually mandatory for TB to
decrease the probability of the emergence of resistant organisms

A
  • Isoniazid
  • Rifampicin
  • Ethambutol
  • Pyrazinamide
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11
Q

tuberculosis (TB)

Second-line Agents

Combination therapy is usually mandatory for TB to
decrease the probability of the emergence of resistant organisms

A
  • Capreomycin
  • Cycloserine
  • Streptomycin

Note: these agents are used treat infections likely to be
resistant to first line agents or when first line agents are
abandoned due to adverse effects.

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12
Q

tuberculosis (TB) Agent

Isoniazid

Pharmacology

A

A prodrug that is activated by bacterial enzymes (katG) and subsequently inhibits synthesis of mycolic acids, an important component of the mycobacterium cell wall
- converted to isoniazid NAD complex, interferes with final step of mycolic acid syth, struggle to make cell wall

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13
Q

tuberculosis (TB) Agent

Isoniazid

AE

A
  • Can cause * hemolytic anemia in people with glucose-
    6-phosphate dehydrogenase deficiency
  • Other adverse effects include allergic skin eruptions,
    fever, hepatotoxicity, arthritic symptoms & vasculitis
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14
Q

tuberculosis (TB) Agent

Rifampicin (aka Rifampin)

Pharmacology

A

Binds to and inhibits DNA-dependent RNA polymerase
only in prokaryotic cells
(not mammalian)
- mycobac cannot transcribe a mRNA to make proteins

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15
Q

tuberculosis (TB) Agent

Rifampicin (aka Rifampin)

AE

A
    • Acute interstitial nephritis (rare)
    • Orange tinge to saliva, tears, sweat
  • (widely distributed in body fluids)
  • Are infrequent but include skin eruptions, fever, GI
    disturbances, & liver damage with jaundice
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16
Q

tuberculosis (TB) Agent

Ethambutol

Pharmacology

A

Only affects mycobacteria (likely via inhibiting arabinosyl transferase to impair mycobacterial cell wall synthesis)
- transfers arabinose residue of arabinoglactan (AG) to mycolic acid, attachments so cell wall cannot be made

17
Q

tuberculosis (TB) Agent

Ethambutol

AE

A
    • optic neuritis (red-green color blindness),
    • peripheral neuropathy
  • rash
18
Q

tuberculosis (TB) Agent

Pyrazinamide

Pharmacology

A

Analog of nicotinamide (prodrug for pyrazinoic acid)

  • Is tuberculostatic at acidic pH and inhibits bacterial
    fatty acid synthesis (likely via inhibiting fatty acid
    synthase that elongates fatty acids)
  • when macrophage engulfs bac, it is contained with lysosomes which has acidic pH that can activate the drug and kill bacteria
19
Q

tuberculosis (TB) Agent

Pyrazinamide

AE

A
  • High doses can lead to serious * hepatic damage (must monitor enzymes)
    • gout: interefere with excretion of uric acid, increase levels
  • GI upset
  • malaise
  • fever
20
Q

tuberculosis (TB) Agent

Capreomycin

Pharmacology

A

A peptide antibiotic thought to act via binding to the 70S ribosomal unit and inhibiting protein synthesis

21
Q

tuberculosis (TB) Agent

Capreomycin

AE

A
    • kidney damage
    • auditory nerve injury (can lead to deafness and
      ataxia)

not given with other antibiotics with ototoxicity

22
Q

tuberculosis (TB) Agent

Cycloserine

Pharmacology

A

Broad-spectrum antibiotic that competitively inhibits bacterial cell wall synthesis by preventing formation of tripeptide side- chains of N-acetylmuramic acid, which is a major building block for peptidoglycan

prevent D-Ala D-Ala dipeptide that forms with N-acetylmuramic acid - tripeptide as building blocks for peptidoglycan

23
Q

tuberculosis (TB) Agent

Cycloserine

AE

A
  • primarily CNS actions, such as headache, irritability,

depression, convulsions & psychotic states

24
Q

Leprosy Agent

Drugs

A
  • Rifampicin
  • Dapsone
  • Clofazimine
25
Q

Leprosy Agent

Dapsone

Pharmacology

A

Chemically related to sulfonamides and thus likely acts via inhibiting bacterial folate synthesis
prevents purine/pyr synth

26
Q

Leprosy Agent

Dapsone

AE

A
    • hemolysis of red blood cells
    • methemoglobinemia
  • anorexia
  • nausea
  • vomiting
  • allergic dermatitis
  • neuropathy

May induce * Lepra reactions (exacerbation of lepromatous regions)

27
Q

Leprosy Agent

Clofazimine

Pharmacology

A

Is a dye with proposed action against leprosy bacilli involving action on DNA (may also be anti-inflammatory)
- can be used with dapsone with can cause inflammation

not really known

28
Q

Leprosy Agent

Clofazimine

AE

A
    • reddish colour of the skin and urine (it’s a dye)
  • lesions can be green bluish
  • GI upset
  • nausea
  • headache
29
Q

Llong-lived as the mycobacterium can survive within macrophages after being phagocytosis, what does this describe?

A

Mycobacterial infections

30
Q

What are the First-line therapies for TB?

A
  • isoniazid
  • rifampicin,
  • ethambutol
  • pyrazinamide
31
Q

Leprosy is generally curable now and treated with what drugs?

A
  • rifampicin
  • dapsone
  • clofazimine
32
Q

Why treatment for TB and Leprosy always involves combination therapy?

A

to reduce risk for drug resistance

233 FINAL (15 decks)

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