How is tuberculosis treated and how does it appear?

Tuberculosis is a common problem that puts a lot of pressure on people's bodies. There are many causes of tuberculosis, which are usually related to pathological factors. The lung function of many people is normal, but because of long-term inhalation of these non-ecological bacteria, huge alveoli are produced, leading to viral engulfment, which gradually leads to lung function infection. In addition, in many areas now, because of poor air quality, people often stay next to chemical plants, inhale waste gas discharged from chemical plants for a long time, and the warm environment are all key factors that lead to tuberculosis. Once tuberculosis appears, it must be isolated and treated to prevent it from being transmitted to family members or loved ones.

Mycobacterium tuberculosis

The most common cause is pulmonary tuberculosis. Because there are a large number of normal flora living in the intestine, Mycobacterium tuberculosis must compete in order to survive and adhere to susceptible cells. There are no normal bacterial flora in the alveoli, and Mycobacterium tuberculosis can be inhaled through droplets or bacteria-containing dust, so pulmonary tuberculosis is more common. 1. Pulmonary infection: Due to the differences in the virulence, quantity and immune status of the infecting bacteria, pulmonary tuberculosis can have the following two manifestations.

(1) Primary infection: mostly occurs in children. There are a large number of macrophages in the alveoli, and a small number of live Mycobacterium tuberculosis are phagocytosed by the macrophages once they enter the alveoli. Because the bacteria contain a large amount of lipids, they can resist lysozyme and continue to multiply, destroying the macrophages. The large number of bacteria released cause inflammation in the alveoli, which is called the primary focus. Due to the lack of specific immunity in the body infected for the first time, Mycobacterium tuberculosis often reaches the hilar lymph nodes through the lymphatic vessels, causing enlargement of the hilar lymph nodes, which is called primary syndrome. At this time, a small amount of Mycobacterium tuberculosis may enter the blood and spread throughout the body, but there may not be obvious symptoms (called latent bacteremia); at the same time, the macrophages in the focus present specific antigens to the surrounding lymphocytes. 3 to 6 weeks after infection, the body produces specific cellular immunity and also develops a hypersensitivity reaction. The phospholipids in the cell walls of Mycobacterium tuberculosis in the lesions, on the one hand, stimulate macrophages to transform into epithelial cells, which fuse with each other or undergo nuclear division to form multinucleated giant cells (i.e., Langhans giant cells); on the other hand, they inhibit the dissolution of tissues by proteases, resulting in incomplete dissolution of lesion tissues and producing caseous necrosis surrounded by epithelial cells, lymphocytes, macrophages and fibroblasts, forming tuberculous nodules (i.e., tuberculous granulomas), which are typical pathological features of tuberculosis. After infection, about 5% can develop active pulmonary tuberculosis. Among these patients, due to low immunity, the disease can spread through the blood and lymphatic system to the bones, joints, kidneys, meninges and other parts, causing corresponding tuberculosis. More than 90% of primary infections form fibrosis or calcification and heal without treatment. However, there is often a certain amount of Mycobacterium tuberculosis lurking in the lesions for a long time, which can not only stimulate the body to produce immunity but also become the source of endogenous infection in the future.

(2) Post-primary infection: The lesions are also most common in the lungs. The pathogens can be foreign (exogenous infection) or originally latent in the lesion (endogenous infection). Since the body already has specific cellular immunity, the characteristics of post-primary infection are that the lesions are mostly localized and generally do not involve adjacent lymph nodes. The caseous necrotic lesions surrounded by cellulose can calcify and heal. If the caseous nodules rupture and drain into the adjacent bronchus, cavities may form and release large amounts of Mycobacterium tuberculosis into the sputum.

In 1990, various types of pulmonary tuberculosis were reported abroad, and 40% of sputum samples were detected to be L type. In recent years, some people have noticed that atypical acid-fast bacteria are found in the lesions but no typical tuberculous nodules are found, which is called "unreactive tuberculosis." The same phenomenon was observed when experimental animals were infected with Mycobacterium tuberculosis L-type. This is because the L-type of Mycobacterium tuberculosis lacks cell wall lipid components and cannot stimulate nodule formation, but only causes lymph node enlargement and caseous necrosis. Judging from the pathological changes alone, it is often mistaken for chronic lymphadenitis. A retrospective study was conducted on 155 paraffin block specimens diagnosed with chronic lymphadenitis. Immunoenzyme staining with BCG antibodies showed 68.9% positive results and 60% acid-fast staining showed acid-fast granules. This indicates that a large proportion of cases are related to Mycobacterium tuberculosis L-type. Attention should be paid to this in clinical practice to prevent missed diagnosis and misdiagnosis.

2. Extrapulmonary infection: In some patients, Mycobacterium tuberculosis can enter the blood circulation and cause intrapulmonary and extrapulmonary dissemination, such as brain and kidney tuberculosis. Sputum bacteria can be swallowed into the digestive tract and can also cause intestinal tuberculosis, tuberculous peritonitis, etc. There are reports abroad that only 2 out of 332 blood samples cultured Mycobacterium tuberculosis, but when these samples were injected subcutaneously into guinea pigs, 12% were infected with tuberculosis. This indicates that most of the Mycobacterium tuberculosis spread in the blood are not the common bacterial type, but an L-type that is difficult to grow. In recent years, there have been many new reports of extrapulmonary tuberculosis, and the detection rate of Mycobacterium tuberculosis L type is higher than that of bacterial type: for example, in 10 cases of tuberculous meningitis in children, 9 cases cultured L type and only 1 case of bacterial type. In the elderly with prostatic hypertrophy, urination was difficult. Postoperative pathological sections showed that acid-fast bacteria L-type accounted for 61.2%, and no case was typical acid-fast bacilli. In patients with chronic prostatitis who tested negative in routine culture, acid-fast bacteria L-type was detected in nearly 1/3. Semen examination of infertile men showed acid-fast bacilli in 7% and acid-fast L-type in 14%. Electron microscopy showed L-type adsorbed on the sperm head and tail. When mice were infected with Mycobacterium tuberculosis L-type, acid-fast bacteria L-type were found in 73% of testicular interstitial inflammation.