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MHD > Mycobacteria > Flashcards

Mycobacteria Flashcards

1
Q

What is the difference between a TB infection and TB disease?

A

TB Infection - Positive skin test
Normal immune function means that only 7-10% of people with TB infection will progress to develop TB Disease

TB Disease is active disease, commonly with upper lung infiltrate or cavitation

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2
Q

Which people are most likely to be infected with TB?

A

Close contacts of an active case

Foreign-born people

Medically underserved, low income

Homeless; Migrant farm workers

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3
Q

Who is more likely to progress from a TB infection to disease?

A

HIV infection (immunocompromised)

Recently infected with TB

Silicosis predisposes to TB

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4
Q

How is TB transmitted?

A

Airborne, so close contacts at high risk

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5
Q

Describe the basic pathogenesis of TB

A

TB gets inhaled and gains access to alveolar macrophages. May spread to regional lymph nodes and has a bloodborne spread.

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6
Q

Describe the basic immune response to TB infection

A

TB antigens swallowed and presented macrophages to CD4 T cells, which release cytokines to activate macrophages. See caseous necrosis with granulomas

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7
Q

What are the two potential outcomes of a Primary TB infection?

A

Latent TB infection (over 90%)

Progression to active TB disease (less than 10%)

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8
Q

What are the potential manifestations of TB Disease?

A

80-90% get an upper lung infiltrate with cavitation

10-15% get extrapulmonary manifestations from initial bloodborne spread (meninges, heart, bone, GU)

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9
Q

What is the Ghon focus?

A

The primary local area of infection, seen on CXR

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10
Q

What si the Ranke Complex?

A

When a Ghon focus becomes calcified, it becomes known as a Ranke Complex

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11
Q

What are common sites for Extrapulmonary TB?

A 
Brain
Epiphyses of long bones
Kidneys
Vertebral bodies
Lymph nodes
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12
Q

Describe the PPD Skin Test

A

Intradermal inoculation of TB antigen. If there was a TB infection, you would see a lump of CD4 lymphocytes having a response a few days later

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13
Q

Describe the Quantiferon Gold Test

A

In vitro blood test that senses how much IFN-y is released when exposed to TB antigen

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14
Q

Describe the NAAT

A

NAAT= Nucleic Acid Amplification Test

Take a sputum sample, submit to lab, they do a PCR-like assay to assess for evidence of TB-like antigen

Rapid diagnosis!

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15
Q

Describe the use of Acid-Fast staining for TB detection

A

This stains the organisms red with blue background staining

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16
Q

Describe the use of bacterial culture in TB diagnosis

A

Liquid media can be more rapid, but in general, culture media can take many weeks to grow.

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17
Q

Where are nontuberculous mycobacteria most commonly acquired?

A

Bioaerosols
Water
Soil
Nosocomial

NOT human-to-human transmission

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18
Q

What are predisposing conditions for a Nontuberculous Mycobacteria infection?

A

Preexisting underlying lung abnormality (COPD, bronchiectasis, IPF, congenital abnormalities)

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19
Q

Where are infections with Nontuberculous Mycobacteria usually contained?

A

They are usually contained in the lung, but they may spread in AIDS patients

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20
Q

You suspect that a patient has TB. Is it more likely that they have TB or an NTM disease?

A

NTM disease

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21
Q

List some basic principles of TB treatment.

A

Multi-Drug Therapy (reducing emergence and enhancing response rates/cures)

Increase adherence

Long duration therapy (at least 6 months)

22
Q 
Isoniazid HCl (INH)
Clinical Use
A

May be used as monotherapy in LATENT TB infection

First line drug for active pulmonary TB, used in combo with at least 2 others

23
Q 
Isoniazid HCl (INH)
MOA
A

Prodrug, activated by catalase peroxidase (TB katG gene)

Targets inhA gene product, inhibiting TB cell wall synthesis (mycolic acid)

24
Q 
Isoniazid HCl (INH)
Resistance Mechanisms
A 
Mutations in either...
katG gene (prevents activation of prodrug to active form)

inhA gene (cell wall/mycolic acid synthesis)

25
Q 
Isoniazid HCl (INH)
Toxicity
A

Hepatotoxicity (monitor baseline liver enzymes and their changes over time)

Neurotoxicity

Hypersensitivity rxns

26
Q

Rifampin

Clinical Use

A

First line drug for TB, always used in combo

Could also be used in combo for S. aureus, N. meningitidis (meninigitis prophylaxis)

27
Q

Why can’t Rifampin be used alone as an antibacterial agent?

A

Rapid development of resistance

28
Q

Rifampin

MOA

A

Inhibits DNA-dependent RNA polymerase encoded by rpoB gene

29
Q

Rifampin

Resistance Mechanisms

A

rpoB mutations

30
Q

Rifampin

Toxicity

A

Hepatotoxicity (increased with INH)
Red discoloration of urine and tears
Influenza syndrome - more common in intermittent dosing
Thrombocytopenia

31
Q

Rifampin

Drug Interactions

A

Interacts with over 100 drugs

Accelerates clearance and reduces effective serum concentrations of….
Warfarin, Estrogen, Anticonvulsants, Antiretroviral drugs

32
Q

Ethambutol

Clinical Use

A

“Helper” drug that inhibits resistance to other drugs

33
Q

Ethambutol

MOA

A

Inhibits TB arabinosyl transferase encoded by embB gene

34
Q

Ethambutol

Toxicity

A 
Optic neuritis (blurred vision, could cause blindness)
Periphral neuropathy
35
Q

Pyrazinamide (PZA)

Clinical Use

A

First line TB drug for the 1st two months of therapy

Good penetration into CSF in tuberculous meningitis

36
Q

Pyrazinamide (PZA)

MOA

A

Prodrug activated y TB pyrazinamidase, encoded by pncA gene

37
Q

Pyrazinamide (PZA)

Toxicity

A

Hepatitis

38
Q

Streptomycin

Clincial Use in TB infection

A

Second line TB drug

39
Q

Streptomycin

MOA

A

Inhibits protein synthesis by binding ribosome

40
Q

Streptomycin

Toxicity

A

Ototoxicity

Nephrotoxicity

41
Q

What is the difference between primary and secondary resistance with TB?

A

Primary- infection of a TB disease that is ALREADY drug resistant

Secondary- an initially susceptuble TB population was selected for resistance

42
Q

What are some factors that can select for drug resistance?

A

Too few drugs

Suboptimal drug dosing or absorption

43
Q

How do you calculate the risk of multi-drug resistance developing?

A

Risk of evolution of resistance to two drugs is the PRODUCT of the risk of the development of resistance to each drug

44
Q

Define Multi-Drug Resistant TB

A

Resistance to both INH and rifampin

45
Q

When you discover that the TB disease is resistant to rifampin, how does that change your therapy?

A

Rifampin resistance eliminates short course (6 mo) TB therapy

Now, the pt will need 18-24 months of therapy

46
Q

What is the typical multi-drug therapy for TB?

A 
4 drug regimen = RIPE in initial phase
Rifampin
INH
PZA
Ethambutol

Continuation phase- only INH and rifampin

47
Q

Describe the use of intermittent therapy for TB

A

2-3x weekly dosing
Only done with Directly Observed Therapy
A nurse visits the patient’s house multiple times weekly to dose them

48
Q

What are the three methods used to treat a LATENT TB infection?

A

INH monotherapy for 9 months

Rifampin monotherapy for 9 months, daily

INH + Rifapentene (once weekly, DOT regimen)

49
Q

Which drugs are used to treat both TB and NTM infections?

A

Rifampin
Ethambutol
Fluoroquinolones
Aminoglycosides

50
Q

Which drugs are used to treat exclusively Non-tuberculous mycobacterial infections?

A

Clarithromycin

Azithromycin

51
Q

What combination of drugs is used to treat leprosy?

A

Rifampin and Dapsone for 12 months, daily

MHD (57 decks)

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