What is the effect of tuberculosis on the immune system?

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Mycobacterium tuberculosis (Mtb), a tubercle bacillus, is the causative agent of TB (tuberculosis). The encounter between Mycobacterium tuberculosis (Mtb), and the host leads to a complex and multifaceted immune response possibly resulting in latent infection, tubercular disease, or the complete clearance of the pathogen.

This can occur by any of a number of clinical conditions that suppress the host immune response, for example, intercurrent viral infection, malnutrition, immunosuppressive therapy, aging, or the use of anti-TNF-α (tumor necrosis factor, a type of chemical messenger) agents.

The recent development of highly specific assays, which measure the release of interferon-γ ( a group of signaling proteins) from blood lymphocytes following in vitro stimulation with specific peptides of the M tuberculosis, that is, the interferon-gamma release assays (IGRAS) have not only been useful in identifying patients with LTBI (Latent tuberculosis infection, patients who do not have any symptoms and can not spread the infection), but also in more accurately differentiating infections caused by M tuberculosis from those caused by other mycobacteria or following BCG (Bacillus Calmette-Guérin) vaccination, which can be misdiagnosed by the less specific TST (Mantoux tuberculin skin test, a method of determining whether a person is infected with Mycobacterium tuberculosis).

The term “granuloma” is derived from the anatomical “granular” appearance of the lesions on gross examination and is a structure consisting mainly of epithelioid macrophages and other inflammatory and immune cells. The classic clinical features associated with active pulmonary TB are as follows (elderly individuals with TB may not display typical signs and symptoms):

1. Cough.

2. Weight loss or anorexia (an eating disorder).

3. Fever.

4. Night sweats.

5. Hemoptysis (blood in sputum).

6. Chest pain (this can result from tuberculous acute pericarditis, a complication of TB).

7. Fatigue.

For diagnosis:

1. Mantoux tuberculin skin test with purified protein derivative (PPD) for active or latent infection (primary method).

2. In vitro, a blood test based on interferon-gamma release assay (IGRA) with antigens specific for Mycobacterium tuberculosis for latent infection.

3. Sputum culture.

4. Specific enzyme-linked immunospot (ELISpot).

5. Nucleic acid amplification tests.

6. Blood culture.

Obtain a chest radiograph to evaluate for possible associated pulmonary findings. The following patterns may be seen:

Cavity formation: indicates advanced infection; associated with a high bacterial load.

Noncalcified round infiltrates may be confused with lung carcinoma.

Homogeneously calcified nodules (usually 5 to 20 mm): tuberculomas (clinical manifestation of tuberculosis, which conglomerates tubercles into a firm lump), representing old infection.

Primary TB: Typically, a pneumonia-like picture of the infiltrative process in middle or lower lung regions.

Reactivation TB: Pulmonary lesions in the posterior segment of the right upper lobe, the apicoposterior (one of the bronchopulmonary segments of the left upper lobe) segment of the left upper lobe, and the apical segments of the lower lobes.

TB associated with HIV disease: Frequently atypical lesions or normal chest radiographic findings.

Healed and latent TB: Dense pulmonary nodules in hilar or upper lobes; smaller nodules in upper lobes.

Miliary TB: Numerous small, nodular lesions that resemble millet seeds.

Pleural TB: Empyema (a collection of pus in the pleural cavity, gram-positive, or culture from the pleural fluid) may be present, with associated pleural effusions.

Extrapulmonary TB:

Biopsy of bone marrow, liver, or blood cultures.

Multidrug-resistant TB ( MDR-TB) is defined as resistance to Isoniazid and Rifampin (anti-tubercular drugs), which are the two most effective first-line drugs for TB. Extensively drug-resistant TB (XDR TB) is a rare type of MDR TB that is, in addition to Isoniazid and Rifampin, resistant to any Fluoroquinolone, and at least one of three injectable second-line drugs (Amikacin, Kanamycin, or Capreomycin). XDR-TB resistance to all anti-TB drugs tested has been reported.

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