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ID Review > Nontuberculous Mycobacterial Infections > Flashcards

Nontuberculous Mycobacterial Infections Flashcards

1
Q

How fast do rapid growers take to grow?

Slow growers?

A

7 days

>14 days

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2
Q

What is the v of NTM?

A

In addition to rate of growth, the organism’s ability to produce yellow pigment with or without exposure to light is assessed.

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3
Q

What are Photochromogens

A

Slow growing and produce a yellow–orange pigment only in the presence of light exposure.

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4
Q

What are Scotochromogens

A

can produce pigment with or without light exposure.

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5
Q

What are Nonchromogens

A

Produce no pigment [all rapid growing NTM are this]

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6
Q

Name the rapidly growing NTM [6]

A

M. abscessus

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7
Q

Name the slow growing Photochromogen NTM [2]

A

M. kansasii

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8
Q

Name the slow growing Scotochromogen NTM [2]

A

M. gordonae

M. scrofulaceum

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9
Q

Name the slow growing Nonchromogen NTM [9]

A 
M. haemophilum
M. malmoense
M. simiae
M. avium
M. intracellulare
M. chimaera
M. ulcerans
M. xenopi
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10
Q

Which NTM need lower incubation temps [28–30°C] [4]

A

M. conspicuum
M. genavense
M. haemophilum
M. marinum

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11
Q

Which NTM needs supplementation with iron [1]

A

M. haemophilum

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12
Q

Which NTM needs supplementation with mycobactin [2]

A

M. paratuberculosis

M. genavense

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13
Q

Which NTM needs supplementation with egg yolk [1]

A

M. ulcerans

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14
Q

Which NTM needs 8-12 week intubation? [2]

A

M. genavense

M. ulcerans

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15
Q

Which NTM has in vivo growth only [1]

A

M. leprae

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16
Q

Which NTM are recovered almost exclusively from municipal water sources? [3]

A

M. kansasii
M. xenopi
M. simiae

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17
Q

Risk factors for NTM disease? [4]

A

bronchiectasis, cystic fibrosis, cigarette smoking, and chronic obstructive pulmonary disease (COPD).

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18
Q

Risk factors for disseminated NTM disease? [4]

A

cell-mediated immunodeficiency (e.g., AIDS and steroids use); genetic syndromes with interferon (IFN)-γ or interleukin (IL)-12 pathway defects.

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19
Q

Is NTM communicable?

A

No.

No evidence of human-human or animal-human transmission.

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20
Q

What are the 5 major clinical syndromes of NTM infection?

A
  1. Pulmonary disease (75%).
  2. Lymphadenitis (5%)
  3. Skin, soft tissue, and bone disease (15%)
  4. Disseminated disease. (5%)
  5. Hypersensitivity (0%)
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21
Q

Species of NTM most associated with pulmonary infection? [3]

A

MAC
M. kansasii
M. abscessus

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22
Q

Species of NTM most associated with lymphadenitis [1]

A

MAC

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23
Q

Species of NTM most a/w skin, soft tissue, and bone disease. [6]

A 
MAC
M. fortuitum group
M. chelonae
M. abscessus
M. marinum
M. ulcerans (rare in United States)
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24
Q

Species of NTM most a/w disseminated infection in an HIV patient [4]

A

M. avium
M. genavense
M. haemophilum
M. kansasii

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25
Q

Species of NTM most a/w disseminated infection in a non HIV patient [2]

A

M. abscessus

M. chelonae

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26
Q

Species of NTM most a/w hypersensitivity pneumonitis [2]

A

Metal workers: M. immunogenum

Hot tub: M. avium

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27
Q

How is lung NTM diagnosed?

A

Combination of BOTH clinical and microbiologic criteria

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28
Q

What are the clinical criteria for diagnosis of NTM lung disease? [2]

A
  1. Pulmonary symptoms, nodular or cavitary opacities on chest radiograph, or an HRCT scan that shows multifocal bronchiectasis with multiple small nodules

AND

  1. Appropriate exclusion of other diagnoses.
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29
Q

What are the microbiologic criteria for diagnosis of NTM lung disease? [3]

A
  1. Positive culture results from at least two separate expectorated sputum samples
    OR
    2.Positive culture result from at least one bronchial wash or lavage
    OR
  2. Transbronchial or other lung biopsy with mycobacterial histopathologic features (granulomatous inflammation or AFB) and positive culture for NTM or biopsy showing mycobacterial histopathologic features (granulomatous inflammation or AFB) and one or more sputum or bronchial washings that are culture positive for NTM.
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30
Q

What are the 2 major species of MAC?

A

M. avium

M. intracellulare.

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31
Q

What type of disease does M. intracellulare cause?

A

NTM lung disease

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32
Q

What type of disease does M. avium typically cause

A

Most common cause of disseminated NTM disease in acquired immunodeficiency syndrome (AIDS) patients.

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33
Q

What are the 2 major types of MAC lung disease?

A

Apical fibrocavitary lung disease

Nodular bronchiectatic disease

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34
Q

Who gets Apical fibrocavitary lung MAC?

A

males in their 40s–50s with history of cigarette smoking ± excessive alcohol use

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35
Q

How does Apical fibrocavitary lung MAC present?

A

Aggressive, untreated, progresses in 1–2 years to extensive lung cavitation with respiratory failure.

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36
Q

How does Nodular bronchiectatic disease lung MAC present?

A

“Lady Windermere Syndrome”: slowly progressive form. Frequently right middle lobe or lingula affected.

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37
Q

Who gets Nodular bronchiectatic disease lung MAC

A

Postmenopausal, nonsmoking, white females.

Scoliosis, thin, pectus deformities*, hypomastia

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38
Q

Treatment of Apical fibrocavitary lung MAC

A

rifampin + ethambutol + macrolide (azithromycin or clarithromycin), daily dosing

Amikacin for first 1-2 months if cavitary disease

Treat for 18-24 months or 12 months after achieving culture-negativity.

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39
Q

Treatment of Nodular bronchiectatic disease lung MAC?

A

rifampin + ethambutol + macrolide (azithromycin or clarithromycin), 3x a week

Treat for 12 months after achieving negative cultures

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40
Q

Presentation of MAC Disseminated Disease?

A

Fever in >80% of cases
Night sweats and weight loss less common
May have abdominal tenderness, hepatosplenomegaly, and lymphadenopathy on exam

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41
Q

Who gets disseminated MAC?

A

AIDs with CD4 <50

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42
Q

Diagnosis of disseminated MAC?

A

Culture of MAC from a sterile site
Blood cultures are positive in 90% of cases (increased to 98% by taking a second sample).

Other possible culture sites: bone marrow, lymph node, or liver

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43
Q

Treatment of disseminated MAC?

A

Macrolide (clarithromycin or azithromycin) + ethambutol ± Rifabutin
ART therapy

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44
Q

Difference between clarithromycin and azithromycin in treated MAC?

A

Clarithromycin has more rapid clearance of MAC.

Azithromycin is better tolerated and has fewer drug interactions.

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45
Q

How long should disseminated MAC treatment continue? [3]

A
  1. Clinical response for at least 3 months.
  2. Good viral load response to ART (<50 copies/mL on two consecutive occasions).
  3. Good CD4 count response to ART (>100 cells/μL on two occasions at least 3 months apart).
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46
Q

What is hot tub lung

A

Hypersensitivity lung disease associated with MAC exposure caused by exposure related to undrained pool or spa with overgrowth of MAC (resistant to disinfectants).

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47
Q

Treatment of MAC Hypersensitivity Pneumonitis

A

Controversial..

  1. removal of the source (e.g., hot tub)
  2. ± steroids,
  3. Short course antimicrobial therapy (3–-6 months) depending on clinical response and disease severity.
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48
Q

Diagnosis of MAC hypersensitivity pneumonitis?

A

Clinical, radiologic, and microbiologic criteria

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49
Q

What is the clinical criteria for MAC hypersensitivity pneumonitis

A
  1. Subacute respiratory symptoms (dyspnea, cough, and fever)
    AND
  2. Hot tub exposure
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50
Q

What is the radiologic criteria for MAC hypersensitivity pneumonitis

A

1.Diffuse infiltrate with nodularity
±
2.Ground glass opacity and mosaic pattern

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51
Q

What is the microbiologic criteria for MAC hypersensitivity pneumonitis

A

MAC isolate in sputum, bronchoalveolar lavage, tissue, and hot-tub water

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52
Q

Procedures a/w M. chimaera infection? [6]

A
  1. Heart valve surgery (replacement or repair)
  2. CABG
  3. Heart transplant
  4. heart–lung transplant
  5. left ventricular assist device (LVAD) implantation
  6. vascular grafts.
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53
Q

Presentation of M. chimaera infection?

A

fever, malaise, weight loss,
Endocarditis, chronic sternal wound infection.
May disseminate to liver, bone marrow, lung, skin, brain, lymph nodes, and bone (spine).

Incubation period median of 19 months (range: 3 months to 5 years).

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54
Q

Lab abnormalities a/w M. chimaera infection

A

Lymphopenia
elevated alkaline phosphatase
severe disseminated infection

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55
Q

Risk factors for M. kansasii infection? [6]

A 
Pneumoconiosis
Chronic obstructive pulmonary disease
Previous mycobacterial disease
Malignancy
Alcoholism
HIV

–> Mostly effects middle aged white men

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56
Q

Reservoir M. kansasii

A

Tap water

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57
Q

Where is M. kansasii most prevalent

A

SE. England, Wales, Central and Southern US

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58
Q

How does M. kansasii present?

A

Pulmonary or disseminated disease.

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59
Q

Describe M. kansasii pulmonary disease

A

Similar to pulmonary TB
Upper lobe predilection and cavitary disease are common
Nodular bronchiectatic lung disease similar to MAC reported

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60
Q

How does disseminated M. kansasii present?

A

Common in those with AIDs

Unlike MAC disseminated disease, 50% of cases also have pulmonary disease.

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61
Q

Treatment of M. kansasii

A

Rifampin, isoniazid, and ethambutol.

12 months from culture negativity.

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62
Q

What drug should be tested to ensure it is sensitive in the treatment of M. kansasii?

A

Rifampin

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63
Q

What are the 3 M. abscessus subsp?

A

abscessus
massiliense
bolletii

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64
Q

Where is M. abscessus prevalent?

A

southeastern US states (Florida to Texas).

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65
Q

How does M. abscessus present?

A

Effects skin, soft tissues, bones.
ulcerations, abscesses, draining sinuses, or nodules
Usually resulting from trauma or surgery (e.g., cosmetic surgeries).

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66
Q

Describe how M. abscessus lung disease prevalence?

A

Third most common cause of NTM lung disease.

Responsible for about 80% of pulmonary disease caused by RGM

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67
Q

Who gets M. abscessus lung disease [risk factors]? [7]

A

white female nonsmokers in their 60s
Bronchiectasis
Prior mycobacterial disease

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68
Q

Presentation of M. abscessus lung disease?

A

Similar to that of MAC lung disease, though only 15% develop cavitary lesions.

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69
Q

What is erythromycin resistance methylase (erm) gene?

A

Gene that causes inducible resistance to macrolides.

M. abscessus subsp. massiliense lacks this gene. Bolletti and abscessus subspecies almost always have this gene.

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70
Q

Treatment principles of M. abscessus

A

Usually 2 out of 3 of the following medications are used..

  1. Tigecycline
  2. Imipenem
  3. Amikacin [TIW to reduce SE]

Generally resistant to..

  1. Linezolid
  2. Moxifloxacin
  3. Cefoxitin

–> Due to resistance usually requires IV therapy.

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71
Q

Management of M. abscessus?

A
  1. drainage of all abscesses and removal of any infected foreign bodies.

Severe skin, soft tissue 4 months.
Bone disease treat 6 months.
Pulmonary disease 12 months from negative culture.

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72
Q

Range of M. chelonae presentation?

A

Skin, soft tissue, and bone disease are the most important clinical manifestations.
Status post plastic surgery with implant placement is classic.
Disseminated skin infection is seen in immunocompromised.
Keratitis have been associated with contact lenses and ocular surgeries (e.g., Lasik).
NTM in the eye is almost EXCLUSIVELY M. chelonae

–> Pulm disease uncommon

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73
Q

Treatment of M. chelonae [4]

A

Macrolide and a companion drug, based on susceptibility testing.

Companion drug options..
tobramycin

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74
Q

How long do you treat M. chelonae infection? [3]

A

Skin and soft tissue infection 4 months.
Bone infection 6 months.
Pulmonary infection 12 months from negative culture.

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75
Q

Risk factors for M. fortuitum infection?

A

Whirlpool footbaths during pedicure procedures in nail salons.

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76
Q

Presentation of M. fortuitum infection?

A

Skin, bone, and soft tissue infections
Responsible for 60% of localized cutaneous NTM infections in previously healthy individuals.
–> NO PREDILECTION FOR IMMUNOCOMPROMISED

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77
Q

Treatment of M. fortuitum? [6]

A

First Line
Quinolones and/or Doxycycline for 4 months

Alt
Minocycline
Aminoglycosides
Sulfamethoxazole–trimethoprim
Macrolides
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78
Q

Why must macrolides in M. fortuitum infection be used with caution?

A

Carries the erm gene

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79
Q

How is M. leprae cultured?

A

In the footpad of immunodeficient mice.

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80
Q

How is M. leprae transmitted? [5]

A 
nasal secretions and respiratory droplets
transplacental
breast-feeding
skin contact  
Armadillos.
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81
Q

How does leprosy present?

A

Hypopigmented skin lesions with hypoesthesia
Lesions can also be erythematous and infiltrative
weakness, autonomic dysfunction, and peripheral nerve thickening.

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82
Q

What are the two subtypes of leprosy

A

tuberculoid (paucibacillary)

lepromatous (multibacillary)

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83
Q

Describe findings of tuberculoid leprosy

A

<5 lesions
Macules or plaques that are hypoesthetic
Limited to skin and nerves

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84
Q

Describe findings of lepromatous leprosy

A

Innumerable lesions which are nodules, papules, macules, or infiltrative dermopathy.
Skin sensation is intact but it may effect multiple systems including eye, nasal mucosa, nerves, kidney, and bone

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85
Q

Describe the pathophysiologic findings of tuberculoid leprosy

A

Well formed granulomas with Absent to rare acid fast bacilli and abundant lymphocytes.

86
Q

Describe the pathophysiologic findings of lepromatous leprosy

A

Abundant acid fast bacilli but NO granulomas and few lymphocytes

87
Q

What is the reversal reaction?

A

Results from the development of exuberant local T-cell-mediated immune response directed at living or dead bacilli. Manifests as increased warmth, erythema, and edema of preexisting lesions and if left untreated can lead to permanent nerve damage.

88
Q

What is Erythema nodosum leprosum

A

Acute development of new subcutaneous nodules that are red, painful, and tender due to complement activation following immune complex deposition.

89
Q

Diagnosis of leprosy?

A

Clinical exam and slit-skin testing is used to make the diagnosis in endemic countries
Histopathological examination of skin biopsy is the gold standard.

–> Serologic tests and PCR if limited use and availability.

90
Q

Treatment of PB leprosy?

Treatment of MB leprosy?

A

Dapsone + Rifampin [monthly] for 6 months

Dapsone + Rifampin [monthly] + Clofazamine [daily and monthly] for 12 months

91
Q

Treatment of reversal reaction?

A

Clofazimine

Steroids

92
Q

Treatment of erythema nodosum leprosum

A

Steroids

Thalidomide

93
Q

What type of disease does M. genavense cause? [1]

A

Disseminated disease in AIDs patient
–> If cultures are negative and disease is suspected this is the likely pathogen as it needs multiple special conditions to grow.

94
Q

If you see M. gordonae what should you think.

A

CONTAMINANT

–> Patient drinking or rinsing with tap water prior to respiratory specimen collection

95
Q

What type of disease does M. immunogenum cause? [3]

A

Central venous catheter-related bacteremia
Hypersensitivity pneumonitis due to metalworking fluid contamination
Skin infection

96
Q

What type of disease does M. mucogenicum cause? [2]

A

Central venous catheter-related bacteremia
Peritoneal catheter-related peritonitis

–> Contaminant if found in lungs

97
Q

What type of disease does M. smegmatis cause? [2]

A

Pulmonary disease in patients with lipoid pneumonia

Rare cause of skin, soft tissue, and bone disease

98
Q

What drug is M. smegmatis resistant to?

A

Macrolides

99
Q

What should you think if M. szulgai is found in culture?

A

IT IS SIGNIFICANT

–> No usually found in environment

100
Q

Type of disease M. terrae complex causes?

A

hand tenosynovitis

101
Q

What type of disease does M. ulcerans cause?

A

Chronic necrotic progressive ulcer of skin and soft tissues (Buruli ulcer).
Think of this in a tropical setting

  • -> Rare in US
  • -> 3rd most common mycobacterial disease world wide [after TB and leprosy]
102
Q

What type of disease does M. xenopi cause?

A

Pulmonary disease with apical cavitation, more commonly in COPD

103
Q

Reservoir for M. xenopi?

A

Hot water systems.

Found in Northern US, Canada, Europe

104
Q

What are the WHO Group A anti-tuberculosis drugs? [2]

A

Moxifloxacin

Levofloxacin

105
Q

What are the WHO Group B anti-tuberculosis drugs? [4]

A

Streptomycin (SM)
Amikacin
Kanamycin
Capreomycin

106
Q

What are the WHO Group C anti-tuberculosis drugs? [4]

A

Ethionamide
Prothionamide
Cycloserine
Linezolid

107
Q

What are the WHO Group D anti-tuberculosis drugs? [4]

A

Para-aminosalicylic acid
Bedaquiline
Carbapenems
Delamanid

108
Q

MOA of aminoglycosides?

A

irreversibly binding to the bacterial 30S ribosome subunit; bactericidal.

109
Q

Role of aminoglycosides in the treatment of MAC? [3]

A

Consider in extensive fibrocavitary pulmonary MAC disease.
Patients who have failed prior drug therapy.
Macrolide-resistant MAC infection.

110
Q

Other possible uses for aminoglycosides in treatment of NTM?

A
  • -> Rifampin resistant M. kansasii

- -> M. chimera infection

111
Q

Aminoglycosides SE [3]

A

Nephrotoxic
Ototoxic
Neuromuscular blockade [myasthenia gravis], esp with kanamycin

112
Q

Monitoring for patients on aminoglycosides? [3]

A

Renal function: weekly or biweekly
Audiology exams: monthly and if eighth nerve toxicity symptoms occur.
Drug levels: weekly

113
Q

Dosing considerations for aminoglycosides?

A
  • -> Renal adjustment

- -> Weight adjustment

114
Q

MOA of Bedaquiline

A

Inhibits the activity of mycobacterial ATP synthase by binding to its c subunit, which prevents the bacterium from generating ATP, ultimately leading to cell death; bactericidal.

115
Q

Clinical use of bedaquiline?

A

Treatment for M. tuberculosis that is extensively drug-resistant

116
Q

Bedaquiline side effects?

A

Nausea, arthralgia, headache, QTc prolongation, hepatotoxicity, increased risk of death.

117
Q

Bedaquiline drug interactions

A

Substrate of CYP3A, and thus drugs that induce or inhibit CYP3A can affect exposure of bedaquiline.

118
Q

Bedaquiline monitoring while on therapy? [3]

A

CMP [LFTs, alk phos, bili]
EKG at baseline than at 2, 12, 24 weeks; DC medications of QTc >500ms
Symptoms of liver issues [fatigue, nausea, anorexia, jaundice, dark urine, liver tenderness]

119
Q

Bedaquiline dosing considerations?

A

TAKE WITH FOOD

–> Enhances absorption 95%

120
Q

MOA of Capreomycin

A

Inhibits bacterial protein synthesis by interacting with the bacterial ribosome.
–> Not well understood

121
Q

Side effects of capreomycin [2]

A

Nephrotoxicity

Ototoxicity

122
Q

Monitoring for Capreomycin [3]

A

audiometric measurements and vestibular function at baseline and during therapy
CMP at baseline and weekly
Magnesium baseline and weekly

123
Q

Describe NTM susceptibility to imipenem

A

> 90% of M. fortuitum group are susceptible
40–60% of M. chelonae
40–60% M. abscessus are susceptible.

124
Q

Side effects of imipenem? [8]

A

seizures, nausea, vomiting, diarrhea, abnormalities in LFTs, neutropenia, eosinophilia, rash.

125
Q

Important drug drug interactions with imiepnem?

A

valproic acid: decreases concentration

Ganciclovir: increases risk of fever

126
Q

Clinical use of cefoxitin in the treatment of NTM?

A

Empiric or definitive treatment of M. abscessus, M. chelonae, and M. fortuitum [RGM]

While awaiting further identification and susceptibility results, cefoxitin may be initiated for empiric treatment of rapidly growing mycobacterial infection; typically used in combination with amikacin and macrolides.

127
Q

Cefoxitin side effects? [5]

A

diarrhea, eosinophilia, rash, hemolytic anemia (rare), pancytopenia (rare)

128
Q

NOTE:

A

No one knows how Clofazimine works

129
Q

Clinical use for Clofazimine

A

Combination therapy for lepromatous (multibacillary) leprosy.

–> Counts as half a drug in a treatment regimen of TB

130
Q

Side effects of clofazimine? [6]

A
  1. abdominal pain, nausea, vomiting, diarrhea
  2. reddish-black or orange skin discoloration within a few weeks of starting clofazimine
  3. Discoloration in hair, urine, sweat, feces, sputum, and other bodily fluids,
  4. reddish-brown corneal and conjunctival discoloration, 5. lymphedema (rare)
  5. exfoliative dermatitis (rare.)

–> Adverse effects related to clofazimine are dose-related and result from its long half-life and tendency to crystallize in fatty tissue. Thus side effects are usually slowly reversible upon discontinuation.

131
Q

Clofazimine drug interactions?

A

co-administration with aluminum-magnesium antacid reduces bioavailability

132
Q

Clofazimine dosing considerations?

A

Administer with food

133
Q

Mechanism of action of Cycloserine

A

Competitively inhibiting at least two bacterial enzymes that either supply D-alanine for or incorporate D-alanine into peptide bridges which assist in maintaining the integrity of the bacterial cell wall.

134
Q

Clinical use of Cycloserine

A

Second line for TB

135
Q

Cycloserine SE? [3]

A

neurotoxicity (convulsion, somnolence, confusion, tremor, vertigo, drowsiness), elevated LFTs, rash.

136
Q

Contraindications to cycloserine use? [5]

A

epilepsy; depression/anxiety, or psychosis; severe renal insufficiency; excessive concurrent use of alcohol.

137
Q

Significant drug interactions to note with cycloserine use? [2]

A
  1. Use with EtOH increases risk of seizures

2. CNS toxicity enhanced with isoniazid

138
Q

Routine monitoring with cycloserine? [2]

A
  1. neuropsychiatric status at monthly intervals

2. Plasma concentration levels

139
Q

How might the neurotoxic effects of cycloserine be mitigated?

A

pyridoxine

140
Q

MOA of dapsone?

A

Acts on folic acid synthesis pathway by inhibiting the enzyme dihydropteroate synthase (DHPS).

141
Q

Clinical use of dapsone in treatment of TB/NTM?

A

Leprosy treatment

142
Q

Dapsone SE? [6]

A 
rash
methemoglobinemia
hemolysis
agranulocytosis
aplastic anemia
hepatotoxicity.
143
Q

Dapsone drug interactions? [2]

A

rifampin increases metabolism.

Probenecid blocks renal excretion

144
Q

Required monitoring for dapsone? [4]

A
  1. CBC with differential (weekly for the first month, monthly for 6 months, then semiannually)
  2. reticulocyte count
  3. liver function tests
  4. monitor for signs of jaundice, hemolysis, or methemoglobinemia.
145
Q

Delamanid MOA?

A

Nitro-dihydro-imidazooxazole drug that inhibits mycolic acid synthesis

146
Q

Clinical use of Delamanid?

A

Third-line agent for MDR-TB
XDR-TB agent
NOT FDA APPROVED

147
Q

Delamanid side effects? [3]

A

rash, nausea, vomiting; QTc prolongation

148
Q

Delamanid contraindications

A
  1. Pregnancy

2. Hypoalbuminemia

149
Q

Delamanid monitoring considerations

A
  1. Baseline and monthly ECGs

2. Serum albumin baseline and monthly

150
Q

Ethambutol MOA

A

Inhibits arabinofuranosyltransferase enzymes that are involved in polymerizing arabinofuranosyl (Araf) residues from DPA into the arabinan components of mycobacterial cell wall arabinogalactan and lipoarabinomannan; bacteriostatic.

151
Q

Clinical use of ethambutol in the treatment of NTM [3]

A

May be included in regimen against..

M. avium complex, M. kansasii, and M. marinum.

152
Q

Ethambutol SE [6]

A

optic neuritis, peripheral neuritis, nephrotoxicity, rash, liver dysfunction, thrombocytopenia (rare).

153
Q

Drug interactions with ethambutol?

A

aluminum hydroxide may decrease the serum concentration

154
Q

Monitoring with ethambutol? [1]

A

visual acuity and color discrimination testing: baseline and monthly

155
Q

What organ metabolized ethemabutol?

A

Kidney

–> DOSE ADJUST

156
Q

MOA of Ethionamide?

A

Interfere with the production of mycolic acids thus disrupting the lipid membrane of mycobacteria.

157
Q

Clinical use of ethionamide?

A

Core second-line agent for treatment of MDR-TB infection.

158
Q

Ethionamide SE? [4]

A
  1. gastrointestinal (i.e., nausea, vomiting, abdominal cramps, diarrhea, metallic taste, anorexia), hepatotoxicity 2. neurologic toxicity (e.g., depression, drowsiness, headache, peripheral neuritis, blurred vision, diplopia)
  2. drug rash with eosinophilia and systemic symptoms (DRESS)
  3. Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN).
159
Q

What reduces neuro SE of ethionamide?

A

pyridoxine

160
Q

Ethionamide monitoring?

A
  1. Baseline and monthly LFTs
  2. Baseline and periodic ophthalmic exams
  3. Blood glucose and TSH
161
Q

MOA of fluoroquinolones?

A

Inhibits DNA gyrase and DNA topoisomerase IV. These two enzymes work together in replication, transcription, recombination, and repair of DNA; bactericidal

162
Q

Role of fluoroquinolones in treatment of TB?

A

Used against drug-resistant tuberculosis or when first-line agents cannot be used because of intolerance.

163
Q

Role of fluoroquinolones in treatment of NTM?

A

Treatment of…
Rifampin-resistant M. kansasii.
M. fortuitum infections

164
Q

NTM generally resistant to cipro? [3]

A

M. chelonae, M. abscessus, and M. immunogenum

165
Q

CNS side effects of fluroquinolones?

A

Dizziness, confusion, hallucinations, seizures, toxic psychosis, insomnia.
Peripheral neuropathy: may be irreversible – discontinue at first signs of sensory or sensorimotor neuropathy.

166
Q

Fluroquinolone dosing consideration

A

Calcium, iron, multivitamins with minerals, antacids, dairy: fluoroquinolones chelate with divalent cations, significantly decreasing bioavailability
–> Administer quinolones 2 hours before OR 6 hours after eating any of the above.

167
Q

Which fluroquinolone does NOT need renal adjustment?

A

Moxifloxacin

168
Q

Role of bactrim in treating NTM? [2]

A

Cutaneous disease caused by M. marinum
–> MAY BE SINGLE AGENT IN MILD DISEASE
Used in combination treatment of M. fortuitum.

169
Q

Important bactrim drug interactions? [2]

A

Warfarin: (attributed to the sulfonamide component of the combination) increases INR.
Rifampin: reduces plasma concentration trimethoprim–sulfamethoxazole

170
Q

NOTE:

A

Cross reactivity with anaphylaxis between antibiotic sulfonamides and nonantibiotic sulfonamides MAY NOT OCCUR [if allergic to lasix, may be okay to use bactrim].

171
Q

MOA of isoniazid?

A

Inhibits synthesis of mycolic acids, a critical component of the lipid-rich mycobacterial cell wall.
Bactericidal

172
Q

How is isoniazide metabolized and what is the significance

A

Liver via hepatic acetylation.
Fast acetylators: may require higher dose for same effect.
Slow acetylators: higher risk of toxicity (neuro and hepatic).

173
Q

Isoniazide SE [4]

A

hepatotoxicity (1%–2.7%), neurotoxicity (<0.2%), nausea, vomiting, diarrhea, rash (2%), acute pancreatitis, drug induced lupus

174
Q

Contraindications to isoniazide use? [3]

A

Acute liver disease
History of liver issues on isoniazide therapy
previous severe adverse reaction (drug fever, chills, arthritis) to isoniazid.

175
Q

Clinical use of linezolid for TB infections

A

Second-line therapy for treatment of M. tuberculosis infection.

176
Q

Clinical use of linezolid for NTM infections

A

Severe pulmonary infections with M. abscessus (both initial and maintenance therapy).

177
Q

Linezolid SE [4]

A

nausea, vomiting, diarrhea.
myelosuppression
peripheral and optic neuropathy
lactic acidosis.

178
Q

Monitoring for patients on linezolid? [2]

A
  1. CBC (weekly)

2. visual function in patients requiring ≥3 months of therapy or in patients reporting new visual symptoms.

179
Q

What is the bioavilability of PO linezolid?

A

100% [IV = PO]

180
Q

MOA of macrolides?

A

Inhibit bacterial protein synthesis by binding to 50S ribosome subunit; bacteriostatic.

181
Q

Clinical use of macrolides in tx of NTM/TB [3]

A
  1. Cornerstone of MAC treatment
  2. rifampin-resistant (RR) M. kansasii.
  3. M. abscessus and other RGM
182
Q

Treatment for secondary MAC prophylaxsis

A

Azithro + ethambutol or rifampin

183
Q

How are macrolides metabolized? [3]

A

Kidneys [Renal dose adjustment]
ALSO induce CYP
Clarithromycin is a potent CYP3A4 inhibitor

184
Q

Macorlide SE [4]

A

GI
Hepatic necrosis and failure [caution with pre-exisitng liver disease]
eosinophilia, fever, skin eruptions
Leukopenia, thrombocytopenia

185
Q

Medications in which use of azithromycin is contraindicated? [4]

A

cisapride, pimozide, ergot alkaloids (e.g., ergotamine, dihydroergotamine), or HMG-CoA reductase inhibitors extensively metabolized by CYP3A4 (e.g., lovastatin, simvastatin)

186
Q

MOA of Para-aminosalicylic Acid (PAS)

A

Structurally related to para-aminobenzoic acid (PABA); its mechanism of action is thought to be similar to the sulfonamides, a competitive antagonism with PABA; bacteriostatic.

187
Q

Clinical use of Para-aminosalicylic Acid (PAS)?

A

Treatment of resistant M. tuberculosis infection in combination with other antituberculous medications.

188
Q

PAS SE? [6]

A

GI
Hypothyroidism
hepatitis, neutropenia, agranulocytosis, renal impairment

189
Q

MOA of pyrazinamide

A

is converted to pyrazinoic acid in susceptible strains of mycobacteria, exact MOA is unknown
More active in acidic environment (e.g., inside macrophages) and against dormant/semi-dormant bacilli.

190
Q

Pyrazinamide SE

A

hepatotoxicity
hyperuricemia
polyathralgia
thrombocytopenia [rare]

191
Q

Contraindications to Pyrazinamide [2]

A

Acute gout

Severe hepatic damage

192
Q

Drug interactions to consider with Pyrazinamide?

A

Increase concentration of cyclosporin

enhance the hepatotoxic effect of rifampin

193
Q

MOA of Rifamycins

A

Inhibit the beta-subunit of DNA-dependent RNA polymerase, blocking elongating RNA transcript. Bactericidal

194
Q

Role of Rifabutin in TB treatment?

A

Used as a substitute for rifampin; reserved for patients who are receiving any medication having unacceptable interactions with rifampin

195
Q

Role of Rifapentine in TB treatment?

A

Used once weekly with isoniazid in special patient populations.

196
Q

Side effects of rifamycins? [6]

A

rash (up to 6% with RIF), hepatotoxicity (1%–2.7%), hemolytic anemia, leukopenia, thrombocytopenia (especially with high-dose therapy), acute renal failure.

197
Q

Rifamycin drug interactions? [9]

A 
macrolides
azoles
caspofungin
oral contraceptives
methadone
protease inhibitors
corticosteroids 
benzodiazepine
Increases INR in warfarin patients
198
Q

MOA of tetracyclines?

A

Inhibit protein synthesis by binding to bacterial 30S ribosome subunits; bacteriostatic.

199
Q

Clinical use of tetracyclines in mgmt of NTM?

A

Treatment of M. leprae infection.

Combination therapy of NTM infections especially RGMs and M. marinum.

200
Q

SE of tetracyclines? [4]

A 
tissue hyperpigmentation
vestibular toxicity (minocycline)
pill-associated esophagitis (doxycycline)
intracranial hypertension (doxycycline).
201
Q

SE of Tigecycline [2]

A

Hepatotoxicity

Pancreatitis

202
Q

Tetracycline drug interactions?

A

Atazanavir + minocycline may lead to decrease in atazanavir plasma concentrations.
tetracyclines chelate with divalent cations, significantly decreasing bioavailability. Separate by at least 2 hours.

203
Q

Of RIPE therapy what is the likelihood of liver toxicity?

A

INH&raquo_space; PZA&raquo_space; Rifampin

204
Q

Risk factor for M. fortuitum lung disease?

A

aspiration

  • -> GERD
  • -> Vomiting.
205
Q

NOTE:

A

Not all with NTM pulmonary disease need treatment.
Some spontaneously regress
If patient’s symptoms [or radiograph] advance or are bothersome - treat

206
Q

Oral medications that generally work against M. abscessus

A
  1. Clofazimine

2. Clarithromycin [only M. massiliense]

207
Q

RGM incubation period for SSTI?

A

2-3 months

208
Q

Treatment of M. marinum?

A

Macrolide + Bactrim
Macrolide + rifampin [alt],

Other agents that work
doxycycline
ethambutol

–> Use 2 drugs in combination for 3-4 months
Often need hand surgery.

209
Q

What exposure is a/w M. chelonae SSTI?

A

Tattoo ink contaminated with tap water

210
Q

If a patient is diagnosed with disseminated MAC with HIV when should you start MAC therapy and HIV therapy?

A

Start MAC therapy first
Wait 2 weeks
Start HAART
–> Reduces risk of IRIS

211
Q

Which medication increases risk of death in NTM in HIV and should be avoided?

A

Clofazimine

212
Q

Most common disseminated NTM in a cancer patient?

A

M. chelonae

ID Review (25 decks)

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