tuberculosis Flashcards
- condition caused by mycobacterium tuberculosis
- slow growing bacteria
- can present as pulmonary illness
tuberculosis
- TB is inhaled and moves down bronchi into middle/lower lobes of lungs
- initial immune reaction releases macrophages, T lymphocytes, IL-1, IL-6, and TNF alpha
- granuloma develops and encases TB
- caseous necrosis develops in center of granuloma leading to ghon focus
- usually asymptomatic
primary TB
hallmark of primary TB
ghon complex
- if pt with latent TB becomes immunocompromised, they may no longer be able to contain the infection
- infection multiplies and spreads
- moves to apices of lungs
- cavitary lesions in apices and necrosis of lung parenchyma
- symptomatic and contagious
reactivation TB
- ghon complex starts to have fibrocalcifications form around it
- keeps TB dormant and not spread
- Ranke complex
- not contagious and can remain dormant for years
latent TB
high risk populations for TB reactivation
HIV, DM, CKD, organ transplant pts, silicosis, immune suppressing drugs, illicit drug use
early symptoms of active TB
malaise, fever, weight loss, severe night sweats, productive cough/hemoptysis
complications of pulmonary TB
pneumothorax
bronchopneumonia
pleural effusion
hemoptysis
PE findings of pulmonary TB
crackles from inspiration or after short cough
look chronically ill, malnourished
- when TB enters the blood stream and spreads to extra pulmonary sites (outside of the lungs)
- disseminated hematogenous spread occurs and the formation of multiple millet seed-sized tuberculosis foci can develop in the lungs
extra pulmonary/miliary TB
TB in pleura
tuberculous pleurisy
central nervous system TB
tuberculous meningitis
pericardium TB
leads to constrictive pericarditis
liver TB
can cause acute hepatitis
adrenal glands TB
leads to inability to produce cortisol –> Addison’s disease
lymphatic system TB
in scrofula of neck
genitourinary system TB
urogenital tuberculosis
bones and joints TB
post’s disease of the spine
tuberculosis arthritis
osteomyelitis in long bones
abscess through skin TB
tuberculous ulcer
extra pulmonary TB PE findings
- subacute–> failure to thrive, FUO, dysfunction of one or more organ systems, night sweats
- acute miliary TB–> multi organ system failure, syndrome of septic shock, acute respiratory distress syndrome (ARDS).
how to diagnose TB
TB skin test
PPD test
Mantoux test
limitations of TB test
- can not distinguish active from latent TB
- read at 48-72 hours
- can’t use with BCG vaccine (bacillus calmette-guerin)***
positive TB test based on what
Less than 5 mm: The result is negative.
5 mm or more: The result is positive for people with certain risk factors, such as HIV, recent contact with someone with TB, or immunosuppression.
10 mm or more: The result is positive for people with additional risk factors, such as recent immigration from a high-TB country, living in a high-risk environment, or working in a high-risk setting.
how to get TB results within 24 hours
interferon gamma release assay
- QuantiFERON TB Gold
- Tspot
what is part of the initial approach to a diagnostic eval of a patient with suspected TB
chest x ray
chest CT
reactivation pulmonary TB classically presents with focal infiltration of the upper lobe:
- apical CASEATING granulomas
- nodular infiltrates
- hilar/paratracheal lymph node enlargement
- ghon and or ranke complexes may be found after healed primary
different ways to get pulmonary TB diagnosis
- 3 consecutive morning sputum specimens
- sputum culture with acid fast stain
- biopsy of caveating granulomas
- DNA/RNA amplification
how to diagnose extra pulmonary TB
biopsy– acid fast smear and culture of tissue, fluid, or drainage
treatment for active TB
6 month regimen
begins with 4 medications x2 months
- isoniazid (INH)
- Rifampin (RIF)
- Ethambutol (EMB)
- pyrazinamide (PZA)
continue treating with INH and RIF for additional 4 months
must treat for at least 3 months beyond negative cultures
treatment for latent TB
isoniazid x 9 months
or
rifampin x 4 months
or
isoniazid and rifapentine weekly x 3 months
or
isoniazid and rifampin daily x 3 months
rifampin side effects
red orange secretions
P450 inducer
isoniazid side effects
peripheral neuritis
pyrazinamide side effects
increased Uric acid
ethambutol
red green discrimination
streptomycin
ototoxic
- regular physician visits, who monitor medication intake and look for signs of medication side effects
- will check sputum smears
- ensures people follow medicine instructions due to long treatment course for TB
directly observed therapy (DOT)
resistant to one first line antituberculous drug, either isoniazid or rifampin
drug-resistant
resistant to isoniazid AND rifampin
multidrug resistant TB
resistant to isoniazid, rifampin, fluoroquinolone, and aminoglycosides and/or capreomycin
extensively drug resistant tuberculosis
options for abbreviated empiric treatment for drug resistant disease
bedaquiline
pretomanid
linezolid plus moxifloxacin
- among the most common opportunistic infections in advanced HIV disease
- occur ubiquitously in the environment (soil and water) (contracted by the bacteria being aerosolized)
- not communicable from person to person
nontuberculous mycobacterial infections
- Most common*
- slow growth
- infects lungs and lymph nodes
- avium complex
- slow growth
- infects lungs, and can lead to disseminated disease
- M. Kansasii
- slow growth
- infects skin and soft tissues
- M. Marinum
- rapid growth
- infects lungs, skin and soft tissues
- M. Abscessus
- rapid growth
- infects skin and soft tissues
- M. chelonae
- rapid growth
- infects skin, soft tissues, and lung
- M. Fortuitum
- disseminated infection
- late stages of HIV
- CD4 count < 50/mcl
- persistent fever and weight loss
NTM outside of lungs
how to treat NTM outside of lungs
clarithromycin or azithromycin + ethambutol +/- rifabutin
2 major phenotypes of NTM lung disease
- nodular/brochiectactic (NB)
- Fibrocavitary (FC)
- typically seen in postmenopausal non smoking white women
- also known as lady windermere syndrome
- pts usually experience many years of progressive respiratory symptoms and recurrent respiratory infections due to unrecognized underlying bronchiectasis
- prolonged cough, fatigue, weight loss
- 50% will not progress
nodular/brochiectatic (NB)
nodular/brochiectatic (NB) CT findings
- bronchiectasis with nodules
- often “tree in bud” appearance
- classically RML and lingual
-typically male pt, over 50
- typically has some form of underlying chronic lung condition
- COPD, silicosis, pulmonary fibrosis
- progressive
- systemic symptoms (fever, fatigue, weight loss, night sweats)
- worse outcome and prognosis than NB type
fibrocavitary (FC)
fibrocavitary (FC) CT findings
fibrocavitary lesions
often upper lobe involvement
diagnosis of pulmonary infection clinical
pulmonary or systemic symptoms
diagnosis of pulmonary infection radiology
nodular or cavitary opacities on CXR,
CT shows bronchiectasis with multiple small nodules
diagnosis of pulmonary infection microbiology
A. positive cx from 2 sputum samples, or
B. positive cx from 1 BAL sample, or
C. lung biopsy with typical histology plus positive cx of tissue biopsy, BAL, or sputum
pulmonary infection treatment
- over half of pts who meet DX criteria progress within 3-5 years
- so start treatment asap
pulmonary (MAC) treatment
3 drug therapy, treated for at least 12 months:
- clarithromycin or azithromycin +
- rifampin or rifabutin +
- ethambutol
pulmonary (M kansasii) treatment
18 months:
- isoniazid
- ethambutol
- rifampin
how to diagnose skin and soft tissue
biopsy and positive culture
skin and soft tissue treatment
surgical debridement with at least two abx for 3 months
- azithromycin
- clarithromycin
- amikacin
- imipenem
- linezolid
- fluoroquinolones
how is lymphadenitis diagnosed
biopsy and culture
lymphadenitis treatment
- surgically with our anti tuberculous therapy
if surgery contraindicated: - azithromycin + rifampin + ethambutol
macrolide resistance can occur if
macrolide mono therapy is given
macrolide resistance treatment
daily ethambutol, rifampin, and clofazimine, augmented by two to six months of IV amikacin
