• Buzz

  • Like sarcoid
    • lymphatics and lymph nodes
  • primary and secondary behave same way
  • different
    • age
    • location

TB of the lung is an infection caused by mycobacterium TB with two phases – an activation phase and a reactivation phase adenopathy a

Inhaled droplets of Mycobacterium

Mycobacterium Tuberculosis (MTB)

• Etymology:
  • The term “tuberculosis” derives from the Latin word “tuberculum,” referring to the nodular lesions (tubercles) seen in the disease.
• AKA:
  • Tuberculosis
  • TB
  • MTB
  • Koch’s Disease
• What is it?
  • Mycobacterium tuberculosis (MTB) is a pathogenic bacterial species belonging to the Mycobacterium genus, primarily causing tuberculosis.
  • It is an obligate aerobe and a slow-growing, acid-fast bacillus.
• Types of Mycobacteria:
  • Mycobacterium tuberculosis
  • Mycobacterium bovis (bovine tuberculosis)
  • Mycobacterium leprae (leprosy)
  • Mycobacterium africanum
  • Mycobacterium microti
  • Nontuberculous Mycobacteria (NTM) such as Mycobacterium avium complex (MAC)
• Caused by:
  • Infection with Mycobacterium tuberculosis, transmitted via airborne droplets.
• Distinction between Latent TB (LTBI) and Active Disease:
  • LTBI:
    • Asymptomatic
    • Positive TST or IGRA
    • No radiographic evidence of active disease
    • Not infectious
  • Active TB:
    • Symptomatic with cough, fever, night sweats, and weight loss
    • Radiographic findings such as cavitation, miliary nodules
    • Infectious
• Forms of Active TB Disease:
  • Pulmonary TB:
    • Most common form
    • Cavitation, consolidation, tree-in-bud nodules
  • Miliary TB:
    • Hematogenous spread leading to widespread tiny nodules
    • Severe form with systemic involvement
  • Endobronchial TB:
    • Spread within the airways
    • Bronchial wall thickening and narrowing
  • Disseminated TB:
    • Involvement of multiple organs
    • Often seen in immunocompromised patients
• Structural Changes:
  • Formation of granulomas
  • Caseating necrosis
  • Cavitary lesions
• Pathophysiology:
  • MTB infects alveolar macrophages.
  • The bacteria can evade immune destruction and form granulomas.
  • Latent TB can persist for years without symptoms but may reactivate.
• Pathology:
  • Granulomas with central caseation
  • Acid-fast bacilli (AFB) on staining
• Diagnosis:
  • Tuberculin skin test (TST)
  • Interferon-gamma release assays (IGRAs)
  • Chest X-ray
  • Sputum AFB smear and culture
  • NAAT and PCR tests
• Clinical:
  • Chronic cough
  • Hemoptysis
  • Night sweats
  • Fever
  • Weight loss
• Radiology:
  • Latent TB:
    • CXR:
      • Parts: Typically normal or may show calcified granulomas
      • Size: Small calcified nodules
      • Shape: Round or oval, with possible retraction of hila and linear nodular changes
      • Position: Upper lobes or apices
      • Character: Non-progressive, with calcified granulomas
    • Associated Findings: Fibrosis, pleural thickening, volume loss, and lymphadenopathy (LAD)
    • CT:
      • Parts: Lungs, often upper lobe involvement with parenchyma and airway involvement
      • Size: Small nodules, <5mm
      • Shape: Nodular with linear and nodular changes, architectural distortion, and hilar retraction
      • Position: Apical and upper lobes, but diffuse in miliary disease
      • Character: Calcification, fibrosis, cicatricial atelectasis, bronchiectasis,
      • Associated Findings: Fibrosis, pleural thickening, volume loss, and lymphadenopathy (LAD)

• Distinction from NTM:
  • MTB is primarily a human pathogen, while NTM species are environmental.
  • MTB often presents with caseating granulomas, while NTM typically involves non-caseating granulomas.
  • MTB is transmissible person-to-person; NTM is generally not transmissible.
• Labs:
  • Latent TB:
    • Tuberculin Skin Test (TST)
    • Interferon-Gamma Release Assays (IGRAs)
  • Active TB:
    • Positive sputum AFB smear and culture
    • Positive NAAT for MTB
    • Elevated ESR and CRP
    • Chest X-ray
    • CT Scan
• Management:
  • • Management:
      • Latent TB:
      •  
        • The criteria for diagnosing LTBI include:
          1. Positive Tuberculin Skin Test (TST): 

          2. Positive Interferon-Gamma Release Assay (IGRA):
        • Isoniazid (INH) monotherapy for 6-9 months
        • Rifampin (RIF) for 4 months (alternative regimen)
        • Isoniazid and Rifapentine weekly for 3 months (3HP regimen)
        • The American Thoracic Society (ATS), Centers for Disease Control and Prevention (CDC), and Infectious Diseases Society of America (IDSA) recommend treating latent TB infection to prevent the progression to active TB disease. This is particularly important in individuals with a positive tuberculin skin test (TST) or interferon-γ release assay (IGRA) who are at increased risk for developing active TB, such as those with HIV infection or other immunocompromising conditions.
          For HIV-infected individuals, the U.S. Public Health Service and IDSA guidelines recommend treatment for latent TB infection if they have a positive TST result (≥5 mm of induration) and no evidence of active TB. Treatment options include isoniazid daily or twice weekly for 9 months, or 4 months of daily rifampin.[2]
          The rationale for treating latent TB is to reduce the risk of reactivation and subsequent transmission of TB. This approach is supported by evidence showing that untreated latent TB can lead to active TB, which has significant public health implications.
      • Active TB:
        • First-line anti-TB therapy:
          • Isoniazid (INH)
          • Rifampin (RIF)
          • Pyrazinamide (PZA)
          • Ethambutol (EMB)
        • Directly observed therapy (DOT) recommended
        • Prolonged treatment for multidrug-resistant TB (MDR-TB)
• Pulmonary Function Tests (PFTs):
  • Not commonly performed but can show restrictive patterns in advanced disease
• Recommendations:
  • Confirm diagnosis with microbiological testing
  • Use standard four-drug therapy for active TB
  • Latent TB infection should be treated with isoniazid or rifampin
• Key Points and Pearls:
  • MTB is primarily an airborne pathogen
  • Cavitary lesions are more typical of post-primary TB
  • Miliary TB presents as diffuse tiny nodules
• Citations:
  • WHO. Global Tuberculosis Report 2021.
  • Centers for Disease Control and Prevention (CDC). Tuberculosis.
  • Sharma SK, Mohan A. Tuberculosis. Indian J Med Res. 2004;120(4):248-276.
• Immediate clearance of the organism
• Primary disease: immediate onset of active disease
• Latent infection

• 

• Reactivation disease: onset of active disease many years following a period of latent infection
  • Consolidation
  • Cavitation
  • Miliary

 

key Dx feature upper or Rt middle lobe involvement initial exudative phase, vol loss instead of exp hypersensitivity rxn causes chronic inflam phase caseation necrosis after 6 wks

Radiology

Primary tuberculosis demonstrates

lymphadenopathy,

consolidation, (CAVITATION UNCOMMON)

pleural effusion, and

miliary nodules

middle lobes

upper portion of lower lobes or lower portion of upper lobes

Ghon lesion, sometimes called Ghon focus,

 initial tuberculous granuloma formed during primary infection and is not radiologically visible unless it calcifies – this occurs

represents a tuberculous caseating granuloma (tuberculoma) and represents the sequelae of primary pulmonary tuberculosis infection.

 

Ghon complex.

is a  Ghon focus alongside ipsilateral mediastinal lymphadenopathy

Ranke complex

is  calcified Ghon complex (Ghon lesion and ipsilateral lymph node) representing a progression of the Ghon complex

radiologically detectable

 

• Feature	Mycobacterium tuberculosis (MTB)	Atypical Mycobacterium (NTM- Non Tuberculous Mycobacteria)   eg avium-intracellulare (MAC)
  Pathogen Type	Mycobacterium tuberculosis complex (MTB)	Mycobacterium avium and Mycobacterium intracellulare
  Transmission	Human-to-human via airborne droplets	Environmental exposure (soil, water, aerosols)
  Primary Reservoir	Humans	Environment (soil, water, birds, animals)
  Virulence and Pathogenicity	Highly virulent, infects healthy individuals	Opportunistic, primarily affects immunocompromised patients (HIV/AIDS)
  Primary Affected Population	General population, especially in endemic areas	Immunocompromised patients (e.g., HIV/AIDS, elderly with structural lung disease)
  Clinical Presentation	Fever, night sweats, cough, hemoptysis, weight loss	Chronic cough, fatigue, weight loss, occasional hemoptysis
  Pulmonary Involvement	Cavitary lesions, consolidation, apical nodules	Bronchiectasis, nodular opacities, tree-in-bud pattern
  CXR Features	Upper lobe cavitation, consolidation, nodules, apical fibrosis	Middle lobe and lingula involvement, nodular opacities, tree-in-bud pattern
  CT Features	– Upper lobe predominant cavitation, apical scarring, tree-in-bud opacities – Patchy consolidation, centrilobular nodules	– Middle lobe and lingula nodular opacities – Bronchiectasis with mucus plugging – Tree-in-bud nodularity
  Extrapulmonary Involvement	Common (e.g., lymph nodes, CNS, bones, GI tract)	Rare, mainly disseminated in immunocompromised hosts
  Histopathology	Caseating granulomas, Langhans giant cells	Non-caseating granulomas or granuloma absence
  Diagnosis	Sputum AFB smear, culture, PCR (GeneXpert)	Sputum culture, PCR, MAC-specific NAAT
  Infectiousness	Highly contagious	Not contagious between humans
  Drug Susceptibility	Requires prolonged treatment, MDR strains exist	Less drug resistance compared to MTB
  First-line Treatment	Isoniazid (INH), Rifampin (RIF), Pyrazinamide (PZA), Ethambutol (EMB)	Clarithromycin or Azithromycin + Ethambutol, Rifabutin
  Treatment Duration	6-9 months (18 months for MDR-TB)	12-18 months or until culture negative for 12 months
  Prevention	BCG vaccination, infection control measures	Avoidance of environmental exposure (e.g., contaminated water)
  Geographical Distribution	Endemic in developing countries	Worldwide, especially in immunocompromised patients
  Complications	Miliary TB, tuberculomas, Pott’s disease	Disseminated disease in AIDS, MAC lung disease
  Immune Response	Delayed-type hypersensitivity (DTH), granuloma formation	Weak immune response, especially in immunocompromised

• 30 year old Female with Positive Sputum
  • multiple tree-in-bud opacities and nodules
    • measuring up to 8 mm in
    • peribronchial vascular distribution in the
    • left upper lobe the,
    • lingula,
    • left lower lobe,
      • withslight surrounding groundglass.
  • several bilateral calcified granulomas.
  • CXR showed

    • 

      

      3 Months Later on Treatment

    • 

      

CT showed

Postprimary tuberculosis 

(aka – reactivation TB and secondary TB)

consolidations that are predominant in the apical and upper lung zones,

nodules, and

 

cavitation

• 

  

  

  

  

   

  Active TB

  • • as primary tuberculosis, developing shortly after infection,
    • or postprimary tuberculosis
      • Stability of radiographic findings for 6 months distinguishes inactive from active disease
    • Primary Active
      • • • lymphadenopathy,
          • consolidation,
          • pleural effusion, and
          • miliary nodules
    • Reactivation
      • consolidations that are predominant in the apical and upper lung zones,
      • nodules
        • tree in bud
      • cavitation

Primary Active and Reactivation

miliary tuberculosis is evenly distributed throughout both lungs

References and Links

• Radiographics
  • Nachiappan, A.C et al    Pulmonary Tuberculosis: Role of Radiology in Diagnosis and Management RadioGraphicsVol. 37, No. 1 2017
  • Rossi, SE et al Tree-in-Bud Pattern at Thin-Section CT of the Lungs: Radiologic-Pathologic Overview RadioGraphicsVol. 25, No. 3 2005

  • Bhalla, A S et al Chest tuberculosis: Radiological review and imaging recommendation  Indian J Radiol Imaging. 2015 Jul-Sep; 25(3): 213–225.
• Radiopaedia

Wiki

• TCV

  • Map
  • Introduction
  • TB Cases