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Microbiology Lecture Slides > Antimycobacterial Therapies II > Flashcards

Antimycobacterial Therapies II Flashcards

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1
Q

TH2-dominated responses lead to

-Extensive tissue damage with many spreading lesions which contain large numbers of bacteria

A

Lepromatous disease

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2
Q

They grow as delicate branching filaments, often seen on microscopic observation of pus from a lesion

-Both tend to cause abscesses

A

Nocardia and Actinomyces

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3
Q

Masses of bacteria in pus are often yellow and called

A

Sulfur granules

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4
Q

Bactericidal against both extracellular and intramacrophage mycobacteria

-Small, water-soluble molecule

A

Isoniazid (INH)

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5
Q

High probability of resistance (~10-6) and is almost always used with other drugs (only exception is prophylactic use)

A

INH

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6
Q

Isoniazid is a pro-drug that is activated by bacterial

A

KatG

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7
Q

Fatty acids are synthesized in two stages in M. tuberculosis. It uses the two enzymes

A

FAS-I and FAS-II

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8
Q

A single multifunctional polypeptide that synthesizes chains up to C16–C26 using acyl-Coenzyme A (CoA) as a carrier

A

FAS-I

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9
Q

A multi-enzyme system that lengthens fatty acid chains to > C52

A

FAS-II

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10
Q

Fab1 (InhA) of FAS-II is the Target of

A

INH-NAD

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11
Q

Fab1 (3-oxoacyl-[acyl-carrier-protein] synthase, InhA) carries out last step in the

A

FAS-II cycle

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12
Q

What are two major side effects of INH?

A

Hepatitis and peripheral neuropathy

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13
Q

The peripheral neuropathy caused by INH is attributable to

A

Pyridoxine deficiency

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14
Q

Metabolism of INH is initiated by acetylation by the liver specific

A

N-acetyltransferase

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15
Q

INH resistance can occur if there are mutations in KatG such that INH-NAD can not be

A

Formed

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16
Q

A complex semi-synthetic antibiotic based on natural antibiotic (rifamycin) isolated from Streptomyces

A

Rifampin

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17
Q

Prevents RNA exit from polymerase by interacting with the large (b) subunit of bacterial RNA polymerase (α2ββ’ωo) and directly blocking the path of the growing RNA

A

Rifampin

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18
Q

Rifampin blocks departure of bacterial RNA polymerase (RNAP) from

A

Gene promoters

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19
Q

Drug resistance to rifampin arises from mutations in the gene encoding the b subunit of

A

RNA Polymerase

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20
Q

Bactericidal against fast growing extracellular mycobacteria in the lung cavity

-Also active against slow growing intracellular mycobacteria

A

Rifampin

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21
Q

Penetrates cerebrospinal fluid adequately if the meninges are inflamed

A

Rifampin

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22
Q

If administrated less then twice weekly – may cause flu-like symptoms (fever, chills, anemia, sometimes acute tubular necrosis, believed to be drug-allergy)

A

Rifampin

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23
Q

Induces cytochrome P450 members including CYP3A => increases elimination of other drugs

A

Rifampin

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24
Q

Rifampin imparts harmless purple or red color to

A

Urine, sweat, and tears

25
Q

Have a higher potency and longer half life than rifampin. Also displays better membrane permeability

A

Rifabutin & Rifapentine

26
Q

Less active in CYP3A induction (particularly rifabutin), this means a better compatibility with other medications (eg., for HIV and arrhythmia)

A

Rifabutin & Rifapentine

27
Q

Shares structurally similarity but not targeting mechanism with INH

A

Pyrazinamide (PZA)

28
Q

PZA is a pro-drug converted to active form by bacterial

A

PcnA enzyme

29
Q

Works synergistically with Rifampin

-A persister killer (also called sterilizer, i.e., bacteriacidal against dormant Mtb but not replicating bacteria)

A

PZA

30
Q

To be used in combination with at least two more other drugs to avoid de facto monotherapy

-Reduces chemotherapy from 9 months to 6 months

A

PZA

31
Q

Enters tubercle bacilli by passive diffusion, where it is converted to POA by PZase/nicotinamidase encoded by the pncA gene

A

PZA

32
Q

Then reaches the cell surface through passive diffusion and a weak (deficient) efflux mechanis

A

POA

33
Q

Upon stress, translating ribosomes are stalled and incomplete polypeptides may be

A

Toxic to the cell

34
Q

The bacterial cell resolves this problem by adding tmRNA to the stalled

A

mRNA

35
Q

This process is called

A

Trans-translation

36
Q

PZA inhibits

A

Trans-translation

37
Q

PZA is converted to the active form pyrazinoic acid (POA) by M. tuberculosis pyrazinamidase (Pzase), which inhibits targets including

A

RpsA

38
Q

POA binding to RpsA interferes with the interaction of RpsA with tmRNA required for

A

Trans-translation

39
Q

Blocks the EmbA and EmbB arabinosyl transfreases that incorporate arabinose into the arabinogalactan layer, thereby weakening the cell wall and making M. tuberculosis susceptible to damage

A

Ethambutol (EMB)

40
Q

Inhibits fast growing extracellular Mtb

-bacteriostatic drug

A

EMB

41
Q

Oral and well absorbed from the gut (reaches blood level of 2-5 mg/ml).

-50% excreted in urine unchanged

A

EMB

42
Q

What are the two major adverse side effects of EMB?

A

Optic neuritis and Red-green color blindness

43
Q

6-10% TB patients in US are

A

HIV positive

44
Q

We never want to give a twice weekly regimen during the continuation phase for a patient who has

A

HIV and TB

45
Q

If rifampin is used to treat TB in a patient with HIV than we must

A

Double or triple the retroviral drug

46
Q

Pathogens (M. avium and M. intracellulare, M. paratuberculosis and possibly other mycobacterial species) are much less susceptible than M. tuberculosis to most

A

Anti-TBs

47
Q

What are the two main antibiotics used to treat MAC infection

A

Azithromycin and clarithromycin

48
Q

A prodrug activated by EthA

-Interferes with cell wall biosynthesis

A

Ethionamide (ETH)

49
Q

Active drug targets FAS-II (similarly to INH) and inhibits mycolic acid synthesis

A

ETH

50
Q

A prodrug targeting dihydrofolate synthesis

A

Para-aminosalicylic acid (PAS)

51
Q

What is the classification of PAS?

A

Bacteriostatic

52
Q

Metabolized in the gut and liver via acetylation. N-acetyl-PAS excreted by the kidney.

-Short half life (1 h) requires 10-12 g/dose

A

PAS

53
Q

What are the major adverse effects of PAS?

A

GI disturbances

54
Q

Produced by soil bacteria

-Structurally related to D-alanine

A

D-cycloserine

55
Q

Drug competitively inhibits alanine racemase and D-alanine ligase

A

D-cycloserine

56
Q

Second line drug with serious side effects: dose related CNS toxicity (headaches, tremors, convulsions, psychosis)

A

Cycloserine

57
Q

A 2nd line anti-TB in US, but still a 1st line drug for developing countries (WHO).

-Employed for treatment of life-threatening TB forms (e.g. meningitis) & drugresistant Mycobacteria bacteria

A

Streptomycin

58
Q

Does not cross mammalian cell membrane (does not enter CNS or macrophages)

A

Streptomycin

59
Q

Amikacin, kanamycin & Capreomycin can be used for strains resistant to

A

Streptomycin

Microbiology Lecture Slides (24 decks)

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