Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
100 Cards in this Set
- Front
- Back
List 5 different mycobacteria that cause human disease.
|
- M. tuberculosis
- M. avium intracellulare complex - M. kansasii - M. chelonae-fortuitum group - M. leprae |
|
Name 4 classes of acid fast organisms.
|
- Mycobacteria
- Nocardia - Legionella - Rhodococcus |
|
Characteristics of waxy coat confers 3 things:
|
- Slow growth
- Evade host defense - Resistance to dying, detergents and traditional antibiotics |
|
T/F: Any of the mycobacteria can cause human disease in any host.
|
False- only M. tuberculosis (others are opportunistic pathogens)
|
|
What makes tuberculosis clinically latent?
|
Organisms live and replicate within macrophages
|
|
What causes cavitary disease in mycobacteria infections?
|
Inflammatory response (NOT toxin from organism)
|
|
Risk factors for TB infection.
|
- High endemic areas
- Male, low SES - Medical conditions: HIV, silicosis, IVDU, DM, ESDR, malignancies - Recent infection with TB |
|
Transmission of TB?
|
- Airborne person-to-person via respiratory droplet nuclei
|
|
What percentage of people who get TB dvelop rectivation within the first 2 years?
|
50% (of the 10% who develop TB)
|
|
Describe latent TB infection.
|
- Positive PPD or IGRA
- No signs or symptoms of TB - Low burden of organisms - Not infectious |
|
Characteristics of TB disease (= tuberculosis).
|
- Signs and symptoms
- Positive culture, histology - Infectious |
|
Presentation of pulmonary TB?
|
- Chroic cough
- Hemoptysis - Drenching night sweats - Weight loss |
|
CXR of pulmonary TB reactivation?
|
Upper lobe fibronodular infiltrates +/- cavitations
|
|
CXR or primary TB?
|
Parenchymal nodules
|
|
Presentation of extrapulmonary TB- pleuritis?
|
Subacute fever with pleuritic chest pain
|
|
How is pleuritic extrapulmonary TB diagnosed?
|
Biopsy
|
|
What is the most common extrapulmonary site of TB?
|
Pleura (= pleuritis: fever with chest pain)
|
|
2nd most common extrapulomary site of TB?
|
Lymph nodes (= lymphadenitis: may not have systemic disease)
|
|
What does miliary TB mean?
|
TB spread lymphohematogenously
|
|
2 situations in which miliary TB can occr.
|
- Progressive primary
- Reactivation |
|
>5mm cutoffs for?
|
- HIV
- Close contact with TB infectious individual - Individual with healed or untreated TB on CXR |
|
>10mm cutoffs for 6 groups of people.
|
- IVDUs
- Medical risk factors for TB - Healthcare workers - Immigrants from highly endemic areas - Local populations that have higher rates - Recent skin test conversions |
|
>15mm cutoffs for?
|
No risk factors
|
|
3 causes of false negative PPD tests.
|
- Anergy
- Improper storage of PPD - Improper administration |
|
3 causes of false positives of PPD tests.
|
- Interpretive error
- Non-TB mycobacteria - BCG |
|
What does IGRA measure?
|
Measured in blood sample after intubation with M. tuberculosis specific proteins
|
|
Pros of IGRA?
|
- Specific for Mtb
- Available within 24 hours - No booster phenomenon |
|
Cons of IGRA?
|
- Cost
- Limited data in kids and immunocompromised |
|
When is the IGRA test preferred?
|
Latent TB infection in people who have received BCG
|
|
How do you diagnose TB disease?
|
CXR (vs. PPD/IGRA for latenet TB)
|
|
Features of reactivation TB on CXR.
|
Upper lobe fibronodular infiltrates with or without cavitation
|
|
Features of primary TB on CXR.
|
Parenchymal nodules and/or hilar adenopathy (HIV, kids)
|
|
What tests might be done to diagnose TB disease?
|
- CXR
- Sputum culture - Mycobacteria culture (takes 8 weeks) - Nucleic Acid Amplification (NAA) |
|
If sputum culture is positive, what confirmatory test will be done for TB?
|
Nucleic Acid Amplification (NAA)
|
|
If sputum is POS, NAA is NEG, does the person still have TB disease?
|
No, indicates non-TB mycobacterial infection
|
|
If sputum is negative and NAA is negative, is TB ruled out?
|
Not necessarily, might be non-infectious, TB is still possible
|
|
If sputum is negative and NAA is positive, does the person have TB disease?
|
YES!
|
|
List 4 first-line anti-TB drugs that are currently available.
|
- Isoniazid
- Rifampin - Pyrazinamide - Ethambutol |
|
Mechanism of INH?
|
Interferes with mycolic acid cell wall synthesis
|
|
How does resistance occur (2)?
|
- Mutations in katG (catalase-peroxidase)
- Mutations in inhA (mycolic acid synthesis regulatory gene) |
|
List 3 main toxicities of INH.
|
- Hepatitis: most important
- Neuropathy - Rash |
|
Greatest risk factor for developing hepatitis while on INH?
|
Age >35 yo (others include daily alcohol use, underlying liver disease, post-partum period)
|
|
How can neuropathy be prevented in people who take INH?
|
Supplement with B6 (= pyridoxine)
|
|
Risk factors for developing neuropathy with INH.
|
- DM
- HIV - Malnourished - Preexisting neuropathy |
|
Taking INH can increase the levels of 3 drugs in particular.
|
- Phenytoin
- Valproate - Carbamazepine |
|
Mechanism of action of rifampin?
|
inhibits DNA-dependent RNA polymerase--> interferes with transcription
|
|
Resistance towards rifampin due to?
|
Mutations in gene encoding beta subunit of RNA polymoerase (rpoB)
|
|
3 main toxicities of rifampin.
|
- Hepatitis
- Hypersensitivity - Orange bodily fluids |
|
Describe hypersensitivity reaction that can occur when taking rifampin.
|
- Flu-like with nephrotics syndrome and thrombocyctopenia
- Cutaneous vasculitis - Flushing, pruritis |
|
What is the biggest problem when giving someone rifampin?
|
Drug interactions: there are >100
|
|
Mechanism of rifabutin?
|
Inhibits DNA-dependent RNA polymerase (same as rifampin)
|
|
Major toxicity of rifabutin?
|
Uveitis: high dose or with fluconazole
|
|
When would you use rifabutin?
|
For HIV patients on protease inhibitors or NNRTIs (because of fewer drug interactions)
|
|
Mechanism of action of PZA?
|
Converts pyrasinamidase to POA (which decreases pH to a level that Mtb can't grow)
|
|
Resistance of PZA?
|
Mutation ingene encoding for pyrasinamidase gene (pncA)
|
|
List PZA toxicities.
|
- Nausea
- Dose-related hepatotoxicity - Arthralgia - Hyperuricemia - Rash |
|
Mechanism of action of ethambutol?
|
Inhibits arabinosyl transferase (which is involved in cell wall synthesis)
|
|
Resistance to ethambutol?
|
Mutation in arabinosyl transferase gene (embB)
|
|
Toxicities of ethambutol?
|
- Dose related optic neuritis
- Hyperuricemia - Rash ** no drug interactions |
|
How would you treat a person with latent TB infection?
|
- INH for 6-9 months or rifampin for 4 months (daily)
|
|
Typical treatment for TB disease.
|
- Intensive phase (2 mo): INH, rifampin, ethambutol,pyrasinamide
- Continuation phase (4 mo at least): INH, rifampin |
|
What if a person is culture positive at 2 months after TB disease treatment?
|
Extend continuation phase for 7 months (therefore, total therapy time= 9 months)
|
|
How do you monitor someone's response to TB therapy?
|
- Clinical response (should feel better within a few weeks)
- Sputum culture and AFB smear: most important! - CXR: least important |
|
What is the most important factor to observe to determine a patient's response to TB therapy?
|
Sputum culture and AFB smear; worry if still positive at 3 months
|
|
How can TB transmission be prevented in healthcare settings?
|
- Administrative controls
- Engineering controls - Use of personal respirators - Periodic skin testing |
|
3 criteria for "non-infectiousness"
|
- Clinically responding to therapy
- 3 negative sputum cultures on separate days - At least 2 weeks of therapy |
|
Name 2 photochromagens.
|
- M. kansasii
- M. marinum |
|
Name 1 scotochromagen.
|
- M. gordonae
|
|
Name 1 non-chromagen.
|
MAC
|
|
Name 3 rapid growers.
|
- M. abscessus
- M. chelonae - M. fortuitum |
|
Which mycobacteria does NOT grow on culture?
|
M. leprae
|
|
How do you diagnose non-TB mycobacteria infections?
|
Culture and histology
|
|
Treatment of MAC infection.
|
- Clarithrymocin or azithromycin
- Rifampin or rifabutin - Ethambutol (maybe amikacin too) ** for first 2 months |
|
Treatment for MAC infection with pulmonary disease?
|
18-24 months
|
|
Prevention strategy for HIV patients and MAC infection?
|
Given when CD4 <50; azithromycin once a week
|
|
Typical treatment for M. kansasii?
|
18 months of INH, rifampin and ethambutol
|
|
2 types of M. leprae.
|
- Tuberculoid
- Lepromatous |
|
Dominant immune response: cellular
|
Tuberculoid
|
|
Lower infectiousness
|
Tuberculoid
|
|
Paucibacillary
|
Tuberculoid
|
|
Dominant immune response: humoral
|
Lepromatous
|
|
Multibacillary
|
Lepromatous
|
|
Higher infectivity
|
Lepromatous
|
|
Hallmark of M. leprae
|
Anesthetic plaque
|
|
Parts of the body where you might see more anesthetic plaques with M. leprae?
|
Cooler parts of the body
|
|
Treatment of paucibacillary leprosy?
|
Dapsone everyday for 5 years
|
|
Treatment of multibacillary leprosy?
|
Dapsone and rifambin for 3 years and then lifelong dapsone
|
|
Branching, filamentous, partially acid fast gram positive organism
|
Nocardia
|
|
Where is nocardia found?
|
Soil
|
|
Portals of entry for nocardia?
|
Lung and skin
|
|
Treatment for nocardia infections?
|
TMP-SMZ for 6-12 months
|
|
Microscopical appearance of rhodococcus?
|
Aerobic gram positive, partialy acid fast
|
|
Where is rhodococcus found?
|
Soil; opportunist
|
|
Disease caused by rhodococcus?
|
Cavitary lung disease with dissemintation
|
|
Treatment of rhodococcus infection
|
Vancomycin or erythromycin with rifampin for 2-6 months
|
|
Where is legionella micdadei found?
|
Pathogen of freshwater amoebae
|
|
2nd most common cause of legionellosis (10%)
|
Legionalla micdadei
|
|
What can L. micdadei cause?
|
Cavitary infiltrates on CXR
|
|
How is L. micdadei treated?
|
Azithromycin or fluoroquinolones for 14-21 days
|
|
What is L. micdadei associated with?
|
Healthcare outbreaks
|