Tuberculosis is one of the most frequent infections worldwide, affecting 1 in 3 people.
The bacteria which are responsible for this is mycobacterium tuberculosis. Despite of tuberculosis being able to infect multiple organs, the most common is pulmonary tuberculosis. If a person infected by just one bacteria, then those can remain inside the body in latent form within the lungs waiting their moment to cause the infection. The main reason to convert from latent tuberculosis into active one is stress, immunocompromised patients, etc.
Just like in the case of a child who was hospitalised. The grandmother brought her eleven-year-old grandson, after an unexpected deterioration and productive cough. The grandmother took care of this child after his mother died a few months after the birth. At the hospital, the child seemed very sick and weak. The child had a prolonged cough, sweating, night sweats and decreased appetite. After a check-up, a fever was also developed. A first assessment and suspicion is that the child suffers from active pulmonary tuberculosis. Knowing this, the symptoms that the child developed, could even be the result of meningitis from tuberculosis.
Since the immune system was not strong, the macrophages released into the lungs immediately began to become infected. There are permanent macrophages in the alveoli of the lungs and their job is to remove foreign particles. The first macrophage located Mycobacterium and with phagocytosis tried to remove it. In most cases, the phagocyte reacts with lysosomes that contain acids, powerful chemicals and enzymes to kill the invading germs. Mycobacterium tuberculosis belongs to the bacteria that have developed a survival mechanism by which they can modify this phagosome so that it cannot fuse with lysosomes, surviving and reproducing in the cells of the lungs. When the macrophage dies, the bacterium is released, re-infecting other macrophages. It also releases the contents into lysosomes, infecting the surrounding tissue and recruiting even more inflammatory cells to the area. Although infected macrophages also have innate immune sensors that not only allow them to recognise that they are invading bacteria, but also trigger the release of cytokines and chemokines. And they are calling for even more immune system defenders, such as neutrophils, dendritic cells and lymphocytes, at the site of infection. Thus, infection with mycobacteria elicits an orchestrated immune response that surrounds the damaged tissue and tries to prevent infection. The end result is called a tuberculous granuloma, a local collection of bacteria that attach to immune cells.
Granulomas multiply, and the immune system tries to react by limiting the infection. And often they can even be too small to be detected on a chest x-ray. If the infection is asymptomatic it is called latent or primary tuberculosis infection.
Causes an inflammatory response and damage to surrounding tissue. This is when the symptoms of fever, weight loss and night sweats began to appear. At the hospital, samples of the child's sputum were found to contain acid-fast bacilli with rapid proliferation. And his chest x-ray confirmed the active disease of pulmonary tuberculosis. The child was treated with four anti-tuberculosis drugs, such as isoniazid, rifampin, pyrazinamide and ethambutol. And fortunately, he began to recover. However, an MRI scan may confirm that there is inflammation in the meninges as well. It is also sometimes accompanied by hydrocephalus or bloating of the abdomen due to obstruction of cerebrospinal fluid flow due to infection.
The molecular pattern on this child's chest x-ray also suggests that the mycobacteria had spread, not only into the lungs but also to other organs, including the brain. You may be surprised to learn that this child's tuberculin skin test came back negative. But cultures of cerebrospinal fluid obtained by lumbar puncture eventually also increased Mycobacterium tuberculosis. And this confirmed that he had tuberculous meningitis. Despite treatment with the four drugs and despite the best efforts of doctors at the hospital, this child died from Mycobacterium infection.
The interaction between the host's immune system and the germ can lead to the various clinical manifestations of tuberculosis infection. The presence of granulomas is one of the hallmarks of Mycobacterium tuberculosis infection. And granulomas are the result of the immune system's efforts to protect the hosts by sinking the germ and developing other immune cells to try to reduce the disease. Mycobacteria have evolved in ways that allow them to colonise, remain, and reproduce in the host despite the immune system's efforts to eradicate them. And the ability of the immune system to remember and recognise this germ during re-exposure provides a powerful diagnostic tool The Tuberculin Skin Test.
Finally, understanding how mycobacteria spread, how they enter and leave the human host, can help prevent local spread of the disease. And knowing the epidemiology of this infection, one third of the world's population is infected with Mycobacterium, although it may be asymptomatic. This can help with greater prevention efforts.