HIV coinfection with tuberculosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The likelihood of getting sick with other infections and diseases is much more in HIV-infected individuals. Tuberculosis (TB) is one of these diseases. TB commonly affects the lungs; however, It can sometimes affects other organs and body parts, such as the brain, heart, kidneys, or spine.
Pathophysiology
- HIV infection weakens the immune system allowing TB infection to activate and turn into active TB disease. Individuals with both TB infection and HIV infection has a very high risk of developing active TB disease. Without treatment, these two infections can work together, to shorten the life span of the person infected with both.
- In patients with advanced HIV disease, there is no sufficient cell-mediated immune response to create cavitation and usually presents with lobar, pleural or disseminated disease.
- TB pleural effusion is exudative, lymphocyte-predominant, and contains high adenosine deaminase levels.
- TB pleural effusion occurs as a result of hypersensitivity reaction to M.tuberculosis, so pleural fluid smear is often negative for acid-fast bacilli and pleural biopsy is the gold standard for confirming the diagnosis.
- Treatment of HIV has to be delayed 1-2 weeks after TB treatment to avoid immune reconstitution inflammatory syndrome (IRIS).
Do all people with HIV get TB disease?
No, but having HIV increases the chance of progressing from Latent TB infection to active TB disease, but not everyone with HIV develops TB. For this reason, people with HIV should be screened for latent TB infection through tests such as tuberculin skin test (TST), interferon-gamma release assay (IGRA), or molecular diagnostics recommended by WHO.[1] But it was found that the risk of TB coinfection is doubled in the first year after seroconversion even before the lymphocyte count starts to decline.So early initiation of ART is recommended.
What is the difference between latent TB infection and active TB disease?
TB is spread through the air from one person to another. The infectious droplets containing the mycobacteria are expelled into the air when a patient with TB disease of the lungs or throat coughs or sneezes. Individuals nearby may get exposed and inhale these mycobacteria and therefore they get infected. However, not everyone gets exposed and infected with TB mycobacteria becomes sick. As a result, two TB-related conditions exist: latent TB infection and active TB disease.
Most people who get exposed to TB mycobacteria and become infected are able to control the bacteria and stop them from growing. Consequently, the bacteria become inactive, but they remain dormant and alive in the body and can get activated later if the immune system is impaired and cannot control the growing of the mycobacterial infection. This is called latent TB infection. With impaired immune system, these mycobacteria begin to multiply in the body and cause active TB disease.
There are an estimated 9 to 14 million persons in the United States infected with TB bacteria. However, it has been reported that most people who have latent TB infection never develop active TB disease. In these people, the TB bacteria remain inactive for a lifetime without causing disease. Individuals with latent TB infection do not feel sick or spread TB mycobacteria to others. Since HIV affects the immune system, people with latent TB infection and HIV coinfection are at much higher risk of developing active TB disease. These mycobacteria begin to multiply in the body and cause active TB disease.
IMMUNOLOGY
The most recently measured CD4+ T-lymphocyte count is the strongest predictor of the risk of tuberculosis in people who are receiving ART. In the PopART trial, it was found that the risk of tuberculosis was 73% lower among people starting ART with a CD4+ T-lymphocyte count of more than 500 per microliter than those starting ART when the CD4+ T-lymphocyte count was 500 or less per microliter.
Progressive CD4+ T-lymphocyte depletion, which is characteristic of untreated HIV infection, is associated with impaired containment of Mycobacterium tuberculosis. CD4+ T lymphocytes produce interferon-γ which activates macrophages infected with M. tuberculosis and facilitate intracellular killing. This is a key step in granuloma formation, which is critical for limiting the growth and spread of M. tuberculosis. Granulomas in patients with hiv show variation from those who donot have it.Some of the variations include:
- reduced numbers of CD4+ T lymphocytes,
- alterations in macrophage activation and maturation (fewer epithelioid and Langhans giant cells),
- increased neutrophil infiltration and necrosis,
- an increase in the viral load.
moreover thy are poorly organised which facilitates dissemination. HIV alters adaptive immune-cell populations and function in multiple ways,preferential depletion of effector memory CCR5+ CD4+ T lymphocytes occurs at mucosal sites. Selective depletion of M. tuberculosis–specific CD4+ T lymphocytes occurs during early HIV infection. HIV-associated chronic immune activation results increased expression of exhaustion markers such as programmed cell death protein 1 (PD-1) and T-cell immunoglobulin and mucin domain 3 (Tim-3), which lead to impaired pathogen-specific responses. Increased type 1 interferon signaling in response to HIV infection may inhibit protective immune responses directed against M. tuberculosis.