There are many causes of cough with weight loss, as follows: a. Mycobacterium tuberculosis belongs to the order Actinomycetes, Mycobacterium genus of the family Mycobacterium, which causes human tuberculosis is mainly human tuberculosis bovine type infection is rare tuberculosis bacillus for aerobic bacteria is not easy to stain by magenta heating stain, even after the use of acidic alcohol rinse can not be decolorized so called acid-resistant bacillus; microscopic examination is slender and slightly curved bacillus is more resistant to the outside world can survive in the shade of wet More than 5 months; but in the sun exposure 2 hours, 5% to 12% cresol soap (Lysol) solution contact 2 to 12 hours, 70% alcohol contact 2 minutes or boiling 1 minute can be killed. The easiest method of sterilization is to directly burn the sputum paper with germs tubercle bacilli, slow growth, proliferation generation takes 15 to 20 hours, growth into visible colonies generally takes 4 to 6 weeks at least also takes 3 weeks. Mycobacterium tuberculosis wall for containing high molecular weight of fatty acids lipids proteins and polysaccharides composed of complex components, and its pathogenic power immune response. In the human body, lipids can cause monocyte epithelial-like cells and lymphocyte infiltration and the formation of tuberculosis nodules; proteins can cause allergic reactions, neutrophil and monocyte infiltration; polysaccharides are involved in certain immune reactions (such as agglutination), Mycobacterium tuberculosis is divided into human, bovine and murine types, the first two types (especially the human standard strain H37Rv) as the main pathogenic bacteria of human tuberculosis. The human type and bovine type bacilli have similar morphology and are both highly pathogenic to guinea pigs, but the human type bacilli are far more immunopathogenic to rabbits than the bovine type bacilli, and the human type bacilli can produce niacin, while the niacin test of the bovine type bacilli is mostly negative. Group A: grow and multiply vigorously, exist outside the cell, strong pathogenicity, infectious, mostly in the early active disease foci within the cavity wall or human cavity easily killed by anti-tuberculosis drugs, especially the best effect of isoniazid, playing a major bactericidal role. Streptomycin and rifampicin are also effective but not as effective as the former. Group B: intracellular bacteria, exist in macrophages, bacteria are protected by acidic cytoplasm, can grow but reproduce slowly, pyrazinamide at pH 5.5 has a better bactericidal effect. Group C: Occasional multiplying bacteria, exist in case of necrotic foci, growth environment is unfavorable to bacteria, tuberculosis bacteria are often dormant, only occasional transient growth and multiplication, only sensitive to a few drugs such as rifampin, group B and C bacteria are recalcitrant bacteria are often the root cause of future relapse, only temporarily dormant, may survive for months and years, also known as persistent bacteria. Group D: dormant bacteria, a small amount of tuberculosis bacteria in the lesion, completely in a dormant state, no pathogenic power and infectious, harmless to humans. Most of them die naturally or are engulfed and killed by any drugs, and rarely recur. The above-mentioned grouping by bacterial growth and reproduction has certain guiding significance for drug selection. Drug resistance is an important biological characteristic of Mycobacterium tuberculosis and is related to the success or failure of treatment. The naturally drug-resistant bacteria continue to grow and multiply, and eventually the drug-resistant bacteria predominate in the flora (sensitive bacteria are eliminated by drugs), and the anti-tuberculosis drugs become ineffective. The very small number of naturally drug-resistant organisms (natural mutations) that occur as a result of genetic mutations usually do not cause serious consequences. Another mechanism of drug resistance is that after contact between drugs and TB bacteria, some bacteria undergo induced mutations and gradually adapt to continue to survive in a drug-containing environment (secondary drug resistance), and the TB bacteria that can grow in solid media containing 1g of isoniazid (INH) or 10g of streptomycin (SM) or 50g of rifampicin (RFP) per milliliter are called drug-resistant bacteria of each drug, respectively. The pathogenicity of INH-resistant strains is significantly reduced in animals, while the pathogenicity of SM-resistant bacteria is generally not reduced, and that of RFP-resistant bacteria is reduced to varying degrees, and the reduction in pathogenicity of TB bacteria resistant to both RFP and INH is more significant than that of those resistant to INH alone. Patients who have not used a drug in the past, but whose sputum bacteria are resistant to the drug, are said to be infected with the original drug-resistant bacteria. The long-term unreasonable use of drugs by the elimination or induction mechanism of drug-resistant bacteria called secondary drug resistance, many of the re-treatment of patients for secondary drug-resistant cases, in recent years to a variety of drug-resistant tuberculosis bacteria are increasing, becoming clinically difficult to cure cases, any drug combination error drug dose is not enough, irregular medication, interruption of treatment or premature discontinuation of drugs can lead to bacterial drug resistance, the consequences of drug resistance is bound to be the recent treatment failure or Therefore, avoiding and overcoming bacterial drug resistance is the key to successful chemotherapy of tuberculosis. About 5% of positive clinical sputum cultures are non-tuberculous mycobacteria (mycobacteria other than Mycobacterium tuberculosis and Mycobacterium leprae), which are also acid-resistant mycobacteria and are widely found in nature. When the body’s immunity is impaired, it can cause intrapulmonary and extrapulmonary infections, and its clinical manifestations are similar to those of tuberculosis. However, most of them are resistant to anti-tuberculosis drugs. The biological characteristics of this non-tuberculous mycobacterium are different from those of M. tuberculosis, such as the ability to grow at 28℃, smooth colonies, negative nicotinic acid test, positive contact test for drug resistance, and no pathogenicity to guinea pigs. Second, the route of infection Respiratory infection is the main route of infection of tuberculosis, droplet infection is the most common source of infection, mainly the sputum of patients with tuberculosis (especially sputum smear-positive untreated), healthy people inhale the droplets emitted by patients coughing and sneezing and become infected. Sputum droplets smaller than 10g can enter the alveolar cavity or float in the air because of their light weight, and sputum droplets with bacteria can be inhaled in poorly ventilated indoor environments for a longer period of time, causing infection. The secondary route of infection is through the gastrointestinal tract into the body, a small number of weak virulent tuberculosis bacteria can be killed by the body’s immune defense mechanism, only when attacked by a large number of virulent tuberculosis bacteria and the body’s immunity is not enough, other routes of infection such as the genitourinary system through the skin are rare. The natural immunity (innate immunity) of human body against TB bacilli is non-specific, while the immunity (acquired immunity) acquired after BCG inoculation or TB infection is specific and can kill the invading TB bacilli or tightly surround them to stop their spread and make the lesions heal. The protective effect of both is relative. On the contrary, measles, diabetes, silicosis, AIDS and other chronic diseases, malnutrition or the use of glucocorticoids and immunosuppressants can reduce the immune function of the body and make it susceptible to tuberculosis infection or reactivate previously stable lesions. The elderly and young children are susceptible to TB infection, which is related to the low cellular immunity in old age and the imperfect cellular immune system in young children. The immunity of tuberculosis is mainly cellular immunity, which is manifested by the sensitization of lymphocytes and the enhancement of phagocyte function. The invading tuberculosis bacilli are engulfed by phagocytes and the antigen information is transmitted to T lymphocytes after processing to sensitize them. The macrophages then become epithelial-like cells and Langhans’ giant cells, and eventually form tuberculosis nodules to confine the lesions. The sensitivity of body tissues to the TB bacterium and its metabolites 4-8 weeks after the invasion of the TB bacterium is called a metabolic reaction. The inflammatory mediators, skin reaction factors and lymphocyte toxins released by another subpopulation of T lymphocytes are associated with local inflammatory exudation and even caseous necrosis, often accompanied by systemic symptoms such as fever, malaise and loss of appetite. At this time, if the skin test with tuberculin (see below) can be positive, the injection of local tissue congestion and edema and a large number of sensitized T lymphocytes infiltration of the body, such cellular immune response to the tubercle bacilli and their metabolites is type IV (late) metamorphosis. Erythema nodosum of the skin, polyarthritis or herpetic conjunctivitis can also occur after infection with M. tuberculosis and are manifestations of tuberculosis allergic reactions, which often occur in patients with primary tuberculosis infection. The peptide polysaccharide complex of the tuberculosis body is related to the reaction, while its wax and tuberculin are related to the metaplasia, causing the antigenic components of the two are different, but immunity and metaplasia often exist at the same time, for example, after BCG vaccination can produce immunity, while the tuberculin reaction (metaplasia) also turns positive, the appearance of the two may also be related to the body’s different T lymphocyte subpopulations produced by the lymphokines Immunity plays a protective role in the body, while metaplasia is usually accompanied by tissue destruction, which is also detrimental to bacteria. The immune and metabolic reactions are sometimes not parallel with the influence of drugs in the complex internal and external environment of the human body, as well as the amount and virulence of the infecting bacteria. In short, the number of invading tuberculosis bacteria, virulence and human immunity, the level of metaplasia determines the development and regression of tuberculosis after infection, human resistance is at a disadvantage when tuberculosis is often easy to develop; on the contrary, the infection is not easy to develop even if the disease is relatively light and easy to cure. (B) Primary infection and reinfection Inoculate guinea pigs with a certain amount of tuberculosis bacteria, the first few days there may be no obvious reaction, about 10-14 days after the injection of local redness and swelling gradually formed ulcers, after a long time. The guinea pigs can easily die, indicating that the guinea pigs are not immune to M. tuberculosis. If the same amount of M. tuberculosis is injected into a guinea pig that has been infected with a small amount of M. tuberculosis 4 to 6 weeks ago, the reaction is obviously different from the above. After the injection, the animal has a high fever for 2 to 3 days, and there is a severe reaction such as redness, swelling, ulceration and necrosis of the injected area, but it heals and crusts soon. Local lymph nodes are not enlarged, and no systemic spread of tuberculosis occurs, nor does it lead to death. This severe local metaplasia caused by reinfection is usually easy to heal and no systemic spread, which is the result of the immunity of the guinea pig to the tuberculosis bacillus. After the first TB infection in the lungs (often in children) (primary infection), the bacteria are carried by phagocytes to the hilar lymph nodes (lymph node enlargement) and can spread systemically (occult bacteremia), which may develop into primary progressive TB disease if the body is immunocompromised. However, in adults (who often had mild tuberculosis infection or BCG vaccination in childhood), the body has a certain immunity, and reinfection at this time does not cause local lymph node enlargement, and systemic dissemination is not easy to occur in the reinfection of local intense tissue, and the reaction lesions are more exudative or even caseous necrosis and dissolution and formation of cavities. I. Basic pathological changes of tuberculosis Human immunity and allergic reactive tubercle bacilli, the number of invasion and its virulence are closely related to the possibility and speed of changing the nature of tuberculosis lesions from one pathological type to another, so the process of lesions is quite complex and the basic pathological changes may not all appear in the lungs of tuberculosis patients. （The early exudative lesions are characterized by congestion and edema and leukocyte infiltration, with neutrophils gradually replaced by monocytes (phagocytes), and exudative lesions of engulfed tubercle bacilli can be seen in large monocytes, usually in the early stages of tuberculosis inflammation or when the lesion worsens. (b) Proliferation-oriented lesions There may be a brief exudative phase at the beginning, when the large monocytes engulf and digest the phospholipid component of the tuberculosis bacilli, causing the large monocytes to become large and flattened, resembling epithelial cells called epithelioid cells, and the epithelioid cells may gather in clusters, and in the center there may be Langhans giant cells, which can transmit the message of the tuberculosis bacilli antigen to the lymphocytes, and there are often more lymphocytes in their periphery. The typical tuberculous nodule, the characteristic lesion of tuberculosis tuberculosis, is also so named tuberculosis nodules in which tuberculosis bacilli are usually not easily found to proliferate, the predominant lesion occurs mostly in cases where the amount of bacilli is low human cell-mediated immunity predominates. (C) metaplasia-based lesions (caseous necrosis) often occur on the basis of exudative or proliferative lesions, if the body’s resistance is reduced, the amount of bacilli too much metaplasia, exudative lesions in the tuberculosis bacilli to win the macrophages continue to multiply, so that the cells cloudy swelling after fatty degeneration, dissolution and fragmentation until cell necrosis inflammation, cell death, release of proteolytic enzymes to dissolve the tissue necrosis, the formation of coagulative necrosis Because of the amount of lipids, the lesion is yellowish gray under visual observation, loose and brittle like cheese, so it is called cheese-like necrosis microscopic examination can be seen as a piece of coagulation dyed eosinophilic red non-nodular necrotic tissue. The above three lesions can co-exist in a pulmonary lesion history, but usually one is the main one, for example, a small amount of caseous necrosis can appear in the center of exudative and proliferative lesions; and the predominantly metaplastic lesions are often accompanied by varying degrees of exudation and the formation of tuberculous nodules. The caseous necrotic lesions are heavily multiplied by tuberculosis bacilli, causing liquefaction and infiltration of neutrophils and large monocytes, and the liquefied caseous necrosis can be partially absorbed and partially discharged from the bronchi to form cavities or cause bronchial dissemination in the lungs. Smaller caseous necrotic or hyperplastic lesions can also be reduced and absorbed after treatment, leaving only slight fibrous scar lesions, which are often accompanied by fibrous tissue proliferation during the healing process, forming striated scar-like caseous lesions, and can also heal due to water loss and contraction and calcium salt deposition, eventually forming calcified foci. When the human body is first infected with tuberculosis bacilli, the bacilli may be phagocytosed by cells and carried to the hilar lymph nodes via lymphatic vessels, and a small amount of tuberculosis bacilli may enter the blood circulation and spread throughout the body, but there may be no significant clinical symptoms (occult bacteraemia). If the necrotic lesions erode the blood vessels, the tubercle bacilli may spread through the blood circulation and cause systemic cornified tuberculosis, including the lungs, such as meningeal bone and kidney tuberculosis. The evolution of tuberculosis pathological changes is related to the immune function of the body and the strength of the local immunity of the lung, with fibrosis being a sign of strong immunity and cavity formation often indicating low immunity.