Acid Fast Bacteria I And Ii

Front 1

List 5 different mycobacteria that cause human disease.

Back 1

- M. tuberculosis
- M. avium intracellulare complex
- M. kansasii
- M. chelonae-fortuitum group
- M. leprae

Front 2

Name 4 classes of acid fast organisms.

Back 2

- Mycobacteria
- Nocardia
- Legionella
- Rhodococcus

Front 3

Characteristics of waxy coat confers 3 things:

Back 3

- Slow growth
- Evade host defense
- Resistance to dying, detergents and traditional antibiotics

Front 4

T/F: Any of the mycobacteria can cause human disease in any host.

Back 4

False- only M. tuberculosis (others are opportunistic pathogens)

Front 5

What makes tuberculosis clinically latent?

Back 5

Organisms live and replicate within macrophages

Front 6

What causes cavitary disease in mycobacteria infections?

Back 6

Inflammatory response (NOT toxin from organism)

Front 7

Risk factors for TB infection.

Back 7

- High endemic areas
- Male, low SES
- Medical conditions: HIV, silicosis, IVDU, DM, ESDR, malignancies
- Recent infection with TB

Front 8

Transmission of TB?

Back 8

- Airborne person-to-person via respiratory droplet nuclei

Front 9

What percentage of people who get TB dvelop rectivation within the first 2 years?

Back 9

50% (of the 10% who develop TB)

Front 10

Describe latent TB infection.

Back 10

- Positive PPD or IGRA
- No signs or symptoms of TB
- Low burden of organisms
- Not infectious

Front 11

Characteristics of TB disease (= tuberculosis).

Back 11

- Signs and symptoms
- Positive culture, histology
- Infectious

Front 12

Presentation of pulmonary TB?

Back 12

- Chroic cough
- Hemoptysis
- Drenching night sweats
- Weight loss

Front 13

CXR of pulmonary TB reactivation?

Back 13

Upper lobe fibronodular infiltrates +/- cavitations

Front 14

CXR or primary TB?

Back 14

Parenchymal nodules

Front 15

Presentation of extrapulmonary TB- pleuritis?

Back 15

Subacute fever with pleuritic chest pain

Front 16

How is pleuritic extrapulmonary TB diagnosed?

Back 16

Biopsy

Front 17

What is the most common extrapulmonary site of TB?

Back 17

Pleura (= pleuritis: fever with chest pain)

Front 18

2nd most common extrapulomary site of TB?

Back 18

Lymph nodes (= lymphadenitis: may not have systemic disease)

Front 19

What does miliary TB mean?

Back 19

TB spread lymphohematogenously

Front 20

2 situations in which miliary TB can occr.

Back 20

- Progressive primary
- Reactivation

Front 21

>5mm cutoffs for?

Back 21

- HIV
- Close contact with TB infectious individual
- Individual with healed or untreated TB on CXR

Front 22

>10mm cutoffs for 6 groups of people.

Back 22

- IVDUs
- Medical risk factors for TB
- Healthcare workers
- Immigrants from highly endemic areas
- Local populations that have higher rates
- Recent skin test conversions

Front 23

>15mm cutoffs for?

Back 23

No risk factors

Front 24

3 causes of false negative PPD tests.

Back 24

- Anergy
- Improper storage of PPD
- Improper administration

Front 25

3 causes of false positives of PPD tests.

Back 25

- Interpretive error
- Non-TB mycobacteria
- BCG

Front 26

What does IGRA measure?

Back 26

Measured in blood sample after intubation with M. tuberculosis specific proteins

Front 27

Pros of IGRA?

Back 27

- Specific for Mtb
- Available within 24 hours
- No booster phenomenon

Front 28

Cons of IGRA?

Back 28

- Cost
- Limited data in kids and immunocompromised

Front 29

When is the IGRA test preferred?

Back 29

Latent TB infection in people who have received BCG

Front 30

How do you diagnose TB disease?

Back 30

CXR (vs. PPD/IGRA for latenet TB)

Front 31

Features of reactivation TB on CXR.

Back 31

Upper lobe fibronodular infiltrates with or without cavitation

Front 32

Features of primary TB on CXR.

Back 32

Parenchymal nodules and/or hilar adenopathy (HIV, kids)

Front 33

What tests might be done to diagnose TB disease?

Back 33

- CXR
- Sputum culture
- Mycobacteria culture (takes 8 weeks)
- Nucleic Acid Amplification (NAA)

Front 34

If sputum culture is positive, what confirmatory test will be done for TB?

Back 34

Nucleic Acid Amplification (NAA)

Front 35

If sputum is POS, NAA is NEG, does the person still have TB disease?

Back 35

No, indicates non-TB mycobacterial infection

Front 36

If sputum is negative and NAA is negative, is TB ruled out?

Back 36

Not necessarily, might be non-infectious, TB is still possible

Front 37

If sputum is negative and NAA is positive, does the person have TB disease?

Back 37

YES!

Front 38

List 4 first-line anti-TB drugs that are currently available.

Back 38

- Isoniazid
- Rifampin
- Pyrazinamide
- Ethambutol

Front 39

Mechanism of INH?

Back 39

Interferes with mycolic acid cell wall synthesis

Front 40

How does resistance occur (2)?

Back 40

- Mutations in katG (catalase-peroxidase)
- Mutations in inhA (mycolic acid synthesis regulatory gene)

Front 41

List 3 main toxicities of INH.

Back 41

- Hepatitis: most important
- Neuropathy
- Rash

Front 42

Greatest risk factor for developing hepatitis while on INH?

Back 42

Age >35 yo (others include daily alcohol use, underlying liver disease, post-partum period)

Front 43

How can neuropathy be prevented in people who take INH?

Back 43

Supplement with B6 (= pyridoxine)

Front 44

Risk factors for developing neuropathy with INH.

Back 44

- DM
- HIV
- Malnourished
- Preexisting neuropathy

Front 45

Taking INH can increase the levels of 3 drugs in particular.

Back 45

- Phenytoin
- Valproate
- Carbamazepine

Front 46

Mechanism of action of rifampin?

Back 46

inhibits DNA-dependent RNA polymerase--> interferes with transcription

Front 47

Resistance towards rifampin due to?

Back 47

Mutations in gene encoding beta subunit of RNA polymoerase (rpoB)

Front 48

3 main toxicities of rifampin.

Back 48

- Hepatitis
- Hypersensitivity
- Orange bodily fluids

Front 49

Describe hypersensitivity reaction that can occur when taking rifampin.

Back 49

- Flu-like with nephrotics syndrome and thrombocyctopenia
- Cutaneous vasculitis
- Flushing, pruritis

Front 50

What is the biggest problem when giving someone rifampin?

Back 50

Drug interactions: there are >100

Front 51

Mechanism of rifabutin?

Back 51

Inhibits DNA-dependent RNA polymerase (same as rifampin)

Front 52

Major toxicity of rifabutin?

Back 52

Uveitis: high dose or with fluconazole

Front 53

When would you use rifabutin?

Back 53

For HIV patients on protease inhibitors or NNRTIs (because of fewer drug interactions)

Front 54

Mechanism of action of PZA?

Back 54

Converts pyrasinamidase to POA (which decreases pH to a level that Mtb can't grow)

Front 55

Resistance of PZA?

Back 55

Mutation ingene encoding for pyrasinamidase gene (pncA)

Front 56

List PZA toxicities.

Back 56

- Nausea
- Dose-related hepatotoxicity
- Arthralgia
- Hyperuricemia
- Rash

Front 57

Mechanism of action of ethambutol?

Back 57

Inhibits arabinosyl transferase (which is involved in cell wall synthesis)

Front 58

Resistance to ethambutol?

Back 58

Mutation in arabinosyl transferase gene (embB)

Front 59

Toxicities of ethambutol?

Back 59

- Dose related optic neuritis
- Hyperuricemia
- Rash
** no drug interactions

Front 60

How would you treat a person with latent TB infection?

Back 60

- INH for 6-9 months or rifampin for 4 months (daily)

Front 61

Typical treatment for TB disease.

Back 61

- Intensive phase (2 mo): INH, rifampin, ethambutol,pyrasinamide
- Continuation phase (4 mo at least): INH, rifampin

Front 62

What if a person is culture positive at 2 months after TB disease treatment?

Back 62

Extend continuation phase for 7 months (therefore, total therapy time= 9 months)

Front 63

How do you monitor someone's response to TB therapy?

Back 63

- Clinical response (should feel better within a few weeks)
- Sputum culture and AFB smear: most important!
- CXR: least important

Front 64

What is the most important factor to observe to determine a patient's response to TB therapy?

Back 64

Sputum culture and AFB smear; worry if still positive at 3 months

Front 65

How can TB transmission be prevented in healthcare settings?

Back 65

- Administrative controls
- Engineering controls
- Use of personal respirators
- Periodic skin testing

Front 66

3 criteria for "non-infectiousness"

Back 66

- Clinically responding to therapy
- 3 negative sputum cultures on separate days
- At least 2 weeks of therapy

Front 67

Name 2 photochromagens.

Back 67

- M. kansasii
- M. marinum

Front 68

Name 1 scotochromagen.

Back 68

- M. gordonae

Front 69

Name 1 non-chromagen.

Back 69

MAC

Front 70

Name 3 rapid growers.

Back 70

- M. abscessus
- M. chelonae
- M. fortuitum

Front 71

Which mycobacteria does NOT grow on culture?

Back 71

M. leprae

Front 72

How do you diagnose non-TB mycobacteria infections?

Back 72

Culture and histology

Front 73

Treatment of MAC infection.

Back 73

- Clarithrymocin or azithromycin
- Rifampin or rifabutin
- Ethambutol (maybe amikacin too)
** for first 2 months

Front 74

Treatment for MAC infection with pulmonary disease?

Back 74

18-24 months

Front 75

Prevention strategy for HIV patients and MAC infection?

Back 75

Given when CD4 <50; azithromycin once a week

Front 76

Typical treatment for M. kansasii?

Back 76

18 months of INH, rifampin and ethambutol

Front 77

2 types of M. leprae.

Back 77

- Tuberculoid
- Lepromatous

Front 78

Dominant immune response: cellular

Back 78

Tuberculoid

Front 79

Lower infectiousness

Back 79

Tuberculoid

Front 80

Paucibacillary

Back 80

Tuberculoid

Front 81

Dominant immune response: humoral

Back 81

Lepromatous

Front 82

Multibacillary

Back 82

Lepromatous

Front 83

Higher infectivity

Back 83

Lepromatous

Front 84

Hallmark of M. leprae

Back 84

Anesthetic plaque

Front 85

Parts of the body where you might see more anesthetic plaques with M. leprae?

Back 85

Cooler parts of the body

Front 86

Treatment of paucibacillary leprosy?

Back 86

Dapsone everyday for 5 years

Front 87

Treatment of multibacillary leprosy?

Back 87

Dapsone and rifambin for 3 years and then lifelong dapsone

Front 88

Branching, filamentous, partially acid fast gram positive organism

Back 88

Nocardia

Front 89

Where is nocardia found?

Back 89

Soil

Front 90

Portals of entry for nocardia?

Back 90

Lung and skin

Front 91

Treatment for nocardia infections?

Back 91

TMP-SMZ for 6-12 months

Front 92

Microscopical appearance of rhodococcus?

Back 92

Aerobic gram positive, partialy acid fast

Front 93

Where is rhodococcus found?

Back 93

Soil; opportunist

Front 94

Disease caused by rhodococcus?

Back 94

Cavitary lung disease with dissemintation

Front 95

Treatment of rhodococcus infection

Back 95

Vancomycin or erythromycin with rifampin for 2-6 months

Front 96

Where is legionella micdadei found?

Back 96

Pathogen of freshwater amoebae

Front 97

2nd most common cause of legionellosis (10%)

Back 97

Legionalla micdadei

Front 98

What can L. micdadei cause?

Back 98

Cavitary infiltrates on CXR

Front 99

How is L. micdadei treated?

Back 99

Azithromycin or fluoroquinolones for 14-21 days

Front 100

What is L. micdadei associated with?

Back 100

Healthcare outbreaks