Tuberculosis of the lungs (lat. Tuberculosis aluminum, cro. Drought) is a chronic, recurrent infectious disease spreading from person to person through the air. It causes Mycobacterium tuberculosis, a slow-growing bacterium resistant to most antibiotics, making it difficult to treat. Despite the availability of effective therapy since the 1950s, there are more tuberculosis cases today than in the rest of recorded history.

If left untreated, tuberculosis can kill approximately half of patients within five years and create significant disease in others. There are estimates that one-third of all persons infected with HIV die of tuberculosis and kills more adults than any other infectious disease. Inadequate tuberculosis therapy can lead to strain formation M. tuberculosis drug-resistant, which is then even more difficult to treat; the drugs needed to treat these strains lead to greater toxicity and higher treatment costs.

Historical notes

Pulmonary tuberculosis

Genetic research suggests that M.tuberculosis present for at least the last 15,000 years. Evidence of tuberculosis in humans dates back to 2400 – 3400 BC, where disease in mummies’ spines was proven. Hippocrates coined the term “this,” or consumption, in 460 BC. Kr., Due to significant weight loss associated with the disease. Despite the frequency of the disease, the cause was unknown.

Until 17, radical and pathological tuberculosis descriptions began to appear in the medical literature. The contagious nature of the disease was suspected as early as 1546. the year when Giralamo Tracastoro wrote that the patient’s bedsheet could contain infectious particles. 1720. Benjamin Marten, an English physician, was the first to suspect that tuberculosis could be caused by “small living things” and that contact with an infected individual could lead to it.

In an important study, a French military doctor Jean-Antoine Villemin demonstrated in 1865. the year that tuberculosis can be transmitted from humans to animals, and hypothesized that a particular organism causes it. It was not until 1882. year, Robert Koch irrefutably proved that M.tuberculosis the cause of tuberculosis.

Despite identifying the causative agent, treatment was not successful. The “sanatorium movement,” which began slowly in the mid-19th century, became widespread during the early to 20th centuries. With bed rest and clean air, some patients had collapsed lungs or had surgery surgically (partially removed). It wasn’t until 1943 that Selman Waksman discovered an ingredient that worked against M.tuberculosis, called streptomycin. Streptomycin was first given to a patient in the eleventh month of 1949, and the patient was cured. Consequently, it was observed that some patients who received streptomycin had only transient improvement because the tubercle bacillus developed drug resistance. It was only with additional anti-tuberculin drugs that effective therapy became a reality.

The causative agent is Mycobacterium tuberculosis

Mycobacterium tuberculosis

The bacilli that cause tuberculosis belong to Mycobacterium tuberculosis with complex. These organisms include Mycobacterium tuberculosis, Mycobacterium Bovis, Mycobacterium africanum, Mycobacterium microti, and Mycobacterium Canetti. Of these mycobacteria, the most recognizable and most common cause is Mycobacterium tuberculosis, although all complex (except M. microti ) members can cause disease (tuberculosis) in humans. The infection usually affects the lungs, but anybody area can be affected. In the United States, approximately 18% of reported cases are extrapulmonary.

M. tuberculosis is a bacterium that grows slowly and forms visible colonies on the substrate after a few days or weeks. The colonies are typically coarse and unpigmented on an agar medium. Tuberculosis, like all mycobacteria, has a thick lipid cell wall that prevents it from staining many colors. Man throws the only real “foundation” for development; M. tuberculosis does not survive in the environment.

The microscopic picture of the tubercle bacillus is very polymorphic. They threw straight or slightly bent sticks, measuring 0.2-0.6 x 1-10 micrometers. Painted by the Ziehl-Neelsen method or fluorochromes, dyes show pronounced acid-alcohol resistance. It has the ability to bind and retain the basic color of carbon-fuchsin even after rinsing with acidic alcohol. Carbol-fuchsin binds to mycolic acid, and the cell wall peptidoglycolipids prevent their repulsion, leaving the bacilli red.

Ways and means of spreading tuberculosis

M.tuberculosis most often penetrates the body through the respiratory system by droplet infection, although other routes may be the site of entry. The respiratory system’s ciliary epithelium removes larger particles, and only an aerosol 1-5 micrometers in size reaches the alveoli. Infectious patients are directly microscopically positive patients (patients who secrete more than 10,000 bacilli in 1 mL of expectorant) with a pronounced irritant cough. In layman’s terms, when someone with tuberculosis coughs, it creates an infectious aerosol that contains bacilli, and the aerosol stays in the air for hours. The most vulnerable are people in close contact with the sick, especially children. The digestive tract of the infection had greater significance in the past, at the time of the bovine tuberculosis epidemic.

Tuberculosis bacilli are most commonly found in the lower areas of the lungs, where ventilation is greatest. A local inflammatory reaction develops in the lungs, but it is most often asymptomatic. Over time, the bacilli penetrate the lymphatic and blood systems and spread throughout the body. After a tuberculosis bacillus infection, two things can happen:

  • A person’s immune system prevents the spread of infection, and the person becomes latently infected;
  • The immune system cannot keep the infection, and the person develops an active form of tuberculosis.

Studies have shown that about 10% of infected people develop an active form of the disease during their lifetime. Of those who develop tuberculosis, approximately 50% will occur in the first 1-2 years after infection, and we call this primary tuberculosis. For the other 50% of infected individuals, the disease develops years or decades later, and this form of tuberculosis is called post-primary or reactivating tuberculosis. If the tuberculosis is pulmonary, as already mentioned, the bacillus can be released into the air, infect other people, and continue the cycle of infections and diseases.


fight against tuberculosis

Tuberculosis remains one of the deadliest diseases globally, affecting a significant portion of the world’s population. It is estimated that about 8-9 million new cases occur each year, and approximately 2-3 million people die from the disease, including approximately one-third of HIV-infected patients. 95% of tuberculosis cases occur in developing countries, where there are no funds and where HIV infection is common. Many cases of tuberculosis originate from an even larger part of the population infected with the causative agent, M. tuberculosis. It is estimated that almost a third of the world’s population is infected.

Areas with a high incidence of HIV infection are particularly vulnerable to an increase in tuberculosis cases, so it is not surprising that the highest incidence rates of tuberculosis occur in sub-Saharan Africa, where the prevalence of HIV infection is very high.

Pathogenesis of tuberculosis

As already mentioned, tuberculosis’s first appearance is called primary or primary tuberculosis. A patient who has already been sensitized to the tubercle bacillus is called postprimary, secondary, or reactivating tuberculosis. M.tuberculosis does not secrete any toxic substances that are harmful to the lungs, but tissue damage occurs due to the body’s reaction to the infection.

Primary tuberculosis

Primary tuberculosis is also called primary infection or childhood tuberculosis and denotes infection in an unsensitized host. The first infection site is called the Ghon foci and is most commonly located subpleural above or below the interlobar fissure. Mycobacteria first multiply unhindered after entering the alveoli until a cellular reaction occurs in which lymphocytes and macrophages dominate very quickly. Macrophages phagocytose bacilli trying to remove them. After digestion of phagocytosed bacilli, macrophages present antigens to lymphocytes, producing characteristic granulomas (tubercles), which are typical of the fourth form of hypersensitivity immune response. Activated macrophages differentiate into epithelioid cells or unite into Langerhans giant cells. At the center of these granulomas, epithelioid cells die, manifested by the formation of caseous necrosis.

The sequence of events in primary pulmonary tuberculosis begins with inhalation of the virulent M.tuberculosis and culminates in the development of cellular immune response to the organism. (A) indicates events in the first 3 weeks after exposure, a (B) events after. A positive tuberculin test accompanies the development of resistance to the organism. [iNOS – inducible nitric oxide synthase; MHC – major histocompatibility complex; MTB – M.tuberculosis; NRAMP1 – natural resistance-associated macrophage protein]

Macrophages play a key role in response to M.tuberculosis. They phagocytose bacilli and thus remove a large number of pathogens. Some bacteria still survive inside macrophages. Because M.tuberculosis is an optional intracellular pathogen, in some cases, M.tuberculosis reproduces within macrophages. Many macro age loaded with bacilli are destroyed, and mycobacteria spread rapidly through the pulmonary lymph vessels to the regional lymph nodes. Tuberculous inflammation also develops in the lymph nodes, and the nodes increase significantly. The primary pulmonary change and the affected regional lymph nodes are called the Ghon complex. If Ghon’s focus is below the pleura, a pleural effusion develops. The outcome of the initial tuberculosis infection depends on many factors that are not fully elucidated but include mycobacteria’s virulence, the number of mycobacteria that enter the lungs, the body’s natural resistance, and the body’s ability to mobilize lymphocytes and begin to form granulomas.

Ghon’s foci usually heal with a connective scar, in which calcifications occur that are seen on X-ray examination. The patient develops cellular immunity to tuberculosis, which is manifested by the tuberculin test’s positivity. If M. tuberculosis enters blood or lymph vessels, the bacilli can spread hematogenously or lymphogenously to other parts of the body. In immunocompetent persons, this pre-immune dissemination has no major consequences. Bacilli cannot grow and remain in various places in the body in a latent form. Healing of the primary Ghon complex does not occur in malnourished, immunosuppressed, or cachectic patients. The inflammation continues and flares up into a progressive primary complex that can progress to massive tuberculous pneumonia. In these patients who cannot mobilize T lymphocytes in defense against infection, tuberculosis bacilli can enter the lymphatic or blood vessels and bronchi and spread to the lungs in the form of miliary tuberculosis. The name comes from the appearance of foci of granulomatous inflammation resembling millet grains (lat. milium – millet). Tuberculous pneumonia and miliary pulmonary tuberculosis can cause death within a few weeks.

Secondary tuberculosis

This form of tuberculosis occurs in patients who have overcome primary tuberculosis and developed cellular immunity against the tubercle bacillus. Inflammation can result from reinfection or reactivation – mostly the reactivation of bacilli left in a latent state in calcified foci of primary tuberculosis. Inflammation usually occurs in the lung tips and much less frequently in other parts of the lungs.

Necrotizing granulomas manifest it. In the central part of the focus, softening occurs, which affects larger parts of the lungs and leads to the formation of cavities called caverns. Pulmonary fibrosis occurs around the cavern. Destruction of blood vessels can cause massive bleeding into the cavities and hemoptysis. After the tubercle bacilli spreads from the lung cavities to other parts of the body, extrapulmonary tuberculosis develops.

Bacilli can spread in three ways: lymphogenic, hematogenous, and aerogenous through the airways. The patient coughs up bacilli that have entered the bronchi and ingested infected sputum can reach the stomach and further into the intestines. Hematogenous and lymphogenic dissemination and reactivation of bacilli cause extrapulmonary tuberculosis in several organs, such as the meninges, kidneys, adrenal glands, epididymis, bones, and soft tissues.


Primary pneumonia is manifested by the acute exudation of inflammatory cells that rapidly organize into granulomas. Granulomas consist of T lymphocytes, epithelioid lymphocytes, and Langhans giant cells. Caseous necrosis develops in the center of the granuloma. Ghon’s focus is usually 1 to 2 cm in diameter and is most often solitary. When the focus is located just below the pleura, fibrinous pleurisy may occur.

In secondary tuberculosis, inflammation occurs in granulomas with central caseous necrosis. Inflammation causes tissue destruction and tuberculoma formation, fibrocaseous masses that resemble tumors. Secondary tuberculosis can affect any organ in the body. For example, cavities form in the lungs and fractures in the bones. In the kidneys, tuberculosis causes papillary necrosis. Destruction of the adrenal glands can cause adrenal insufficiency (Addison’s disease). In the epididymis, tuberculosis causes the formation of palpable nodules. Such granulomas can cause an obstruction and prevent sperm from leaking out of the testicles.

Brain tuberculomas may be clinically similar to brain tumors. In the meninges, tuberculosis can impede the absorption of cerebrospinal fluid and cause hydrocephalus. On the skin and mucous membranes (e.g., larynx or intestines), tuberculosis causes nodules or ulcerations. The macroscopic picture in HIV-infected patients is often atypical; granulomas may be absent or vaguely limited and free of necrosis.

Clinical picture

Primary tuberculosis rarely causes symptoms. When symptoms do occur, they are usually associated with local complications. Tuberculosis is asymptomatic until the disease progresses. When it progresses, the symptoms are not specific. They are localized to the site (or sites) affected by the disease. Systemic symptoms include fatigue, fever, anorexia, weight loss, and night sweats.

Symptoms of pulmonary tuberculosis

Inactive pulmonary tuberculosis is asymptomatic, and may have a range of radiographic features. Active tuberculosis may be asymptomatic initially, but as the disease progresses, symptoms such as cough and sputum, shortness of breath, and hemoptysis (less common) may occur.

Hemoptysis can occur with active or inactive (cured) pulmonary tuberculosis. Bloody sputum is not uncommon in any of these cases. Massive hemoptysis is fortunately much rarer.


In order to diagnose tuberculosis, it must first be suspected according to the above symptoms: fever, night sweats, loss of appetite and weight, and cough (which usually lasts 3 or more weeks). The symptoms of extrapulmonary tuberculosis have been reported to vary depending on the location.

When tuberculosis is suspected, it must be assessed whether the patient has had contact with a person with infectious tuberculosis, whether he or she has had tuberculosis or a latent infection in the past, and what risk factors the patient has, particularly HIV infection.

Physical examination may show enlarged lymph nodes, especially in the neck area. Weight loss is always present in the diagnosis of tuberculosis, but none of these signs can confirm or rule out tuberculosis.

The first step in diagnosis is an X-ray of the lungs. Abnormalities of the upper lung lobe with cavities will be present on the images in most adults. In children and patients with HIV infection, there is often an enlargement of the lymph nodes and the disease can be seen in the inferior lung zones.

When tuberculosis is suspected, three sputum samples are taken, which are analyzed for M.tuberculosis. Samples are taken on three different days, usually in the morning. Alternatively, samples may be taken every eight hours with at least one sample taken early in the morning. In patients who cannot cough up sputum, coughing can be induced by inhalation of hypertonic NaCL solution (3% to 10%).

Bronchoscopy may also be performed if respiratory specimens cannot be obtained by coughing, although the chance of identifying M. tuberculosis in bronchoscopic specimens is similar to the chance of identification obtained by sputum induction.

Younger children often cannot cough up sputum and bronchoscopy has been shown to have a relatively small chance of identifying M. tuberculosis. Therefore, aspirates (samples) of gastric fluids are taken and then cultured. Usually, the aspirate is taken early in the morning before the child gets out of bed or eats.

In patients with extrapulmonary tuberculosis, clinical specimens are obtained from the affected site. By aspiration or biopsy of cervical lymph nodes there is a high probability of finding bacilli on smear or in culture, while the chance of finding bacilli in cerebrospinal fluid is relatively low. Similarly, the likelihood of getting mycobacteria from pleural fluid is low, but the chance can be increased (to almost 80%) by pleural biopsy.

In much of the world, sputum samples (and other respiratory samples) are examined by smear and microscopic examination to find evidence of acid-fast methodo-staining bacilli (AFB). Most mycobacteria are AFB, so the presence of AFB in clinical specimens provides only preliminary evidence of tuberculosis. Moreover, most cases of smear tuberculosis give negative results. In areas with a high incidence, a positive AFB smear is almost always evidence of tuberculosis. However, in low-incidence areas, a positive AFB smear is likely due to non-tuberculous mycobacteria. Consequently, fluorochrome staining with auramine-rhodamine is preferred because it is faster and more sensitive than traditional methods, such as the Ziehl-Neelsen or Kinyoun method.

The definitive diagnosis of tuberculosis depends on the isolation of M.tuberculosis from a person suspected of having the disease. Respiratory culture cultures will detect M.tuberculosis in more than 85% of cases of pulmonary tuberculosis, with results becoming available within 7 to 14 days in liquid cultures or 3 to 8 weeks on solid medium. However, cultures are often not available in poor countries, which often have the highest incidence of tuberculosis.

When growth is detected, the type of mycobacteria must be identified. Identification can be done biochemically, but takes 6 to 12 weeks. Faster assays, such as the AccuProbe® assay, that detect specific nucleic acid sequences in culture material can identify the species in 2 to 4 hours.

Nucleic acid amplification assays, such as PCR and other DNA or RNA amplification methods, can facilitate rapid detection of M. tuberculosis directly on a sputum sample (without waiting for culture). Several such commercial kits are available on the market [Amplified MTD (Mycobacterium Tuberculosis Direct) test (Gen-Probe, Inc., San Diego, CA) and Amplicor MTB test and COBAS Amplicor MTB test (Roche Molecular Diagnostics, Pleasonton, CA)]. These tests can quickly determine if there is a clinical pattern of nucleic acid from M.tuberculosis compared to other types of mycobacteria. In general, both tests give the best results in AFB positive smears. SAMO is an Amplified MTD test suitable for testing AFB positive and negative samples.

In individuals who have a positive culture, a drug susceptibility test is performed to determine if there is drug resistance. By culturing bacilli in media containing different concentrations of antituberculin drugs, it can be determined which drugs act against the strain of the bacterium with which the patient is infected. Therefore, individual therapy is “tailored”.

Diagnosing latent infection

For decades, evidence of skin reactivity to tuberculosis antigens has been used to diagnose latent TB infection (LTBI). The Mantoux tuberculin skin test (TST) was the standard method of identifying individuals with LTBI. Mantoux tubeculin skin tests are performed by injecting 0.1 mL of purified protein derivative (PPD) intradermally on the volar surface of the forearm. People who are educated to read skin tests should look at them 48 to 72 hours later. The diameter of the affected area should be measured transverse to the long axis of the forearm. The amount of erythema (redness) is not measured.

The appropriate limit for defining a positive TST depends on the risk factors for tuberculosis. For individuals who are severely immunocompromised, have scars on chest X-ray, or have had recent contact with infected individuals, a reaction size ≥ 5 mm is considered positive. If a person does not have risk factors for tuberculosis, a reaction ≥ 15 mm is required to have a positive case, and for all other cases in between, ≥ 10 mm is considered positive.

The delayed type of hypersensitivity reaction to tuberculin may decrease over time. If a person’s skin is tested years after the initial infection, the reaction may be false negative. However, TST can stimulate the immune “memory” of tuberculin antigens (“boost” reactions) so that repeated TST will be positive. This is considered a real positive reaction. Repeated skin testing in persons not infected with M.tuberulosis should not induce a positive TST result. The “boost” reaction can sometimes be misinterpreted as a change from a negative to a positive reaction, which would suggest a recent infection with M.tuberculosis. In reality, the person had not been infected recently, but had been infected in the past, and her immune system had “forgotten” that she had previously seen tuberculosis antigens.

Two-step testing is used to reduce the possibility of a “boosted” reaction being misinterpreted as a recent infection. In these two steps, the initial TST is performed and read after 48 to 72 hours. Whoever classifies a TST reaction as negative, another TST is done after 1-3 weeks, and reads as usual. If the second TST is negative, the patient is considered TST negative and uninfected with M.tuberculisis. However, if the second TST is positive, the patient is considered to have LTBI, which of course is not the result of a recent infection. A positive reaction to a previous TST would be considered a new infection. Two-step testing is recommended in the initial assessment of adults who will be retested periodically, such as those employed in health care activities.

As with any other test, there may be false positives and false negatives. False-negative results occur in people who are immunocompromised (for example, HIV-infected, or patients on immunosuppressive drugs), in people who have recently had TB infection, in very young children (< 6 months), a few weeks after vaccination with live viruses, etc. False positive tests can be caused by cross-reactive antigens such as antigens containing other mycobacterial species and the BCG vaccine (Bacillus of Calmette and Guérin). Because the BCG vaccine is widely used in countries with a high incidence of TB, it is a common cause of false-positive TST results.

Recently, new blood tests called “interferon-gamma release assays” have been developed to identify latent infections. These tests utilize specific antigens that are found almost exclusively in organisms in the M.tuberculosis complex and not in M.bovis BCG (the organism used to make the BCG vaccine). Therefore, unlike TST, past BCG vaccination should not cause false positive results.

Treatment of tuberculosis

Drug resistance for M.tuberculosis arises through random mutations in the genome of the organism. In any population of M. tuberculosis, the frequency of these mutations varies depending on the drug. If a patient with active tuberculosis is treated with only one drug, drug-resistant mutants survive, grow, and become the predominant population. Studies have shown that if a patient with pulmonary tuberculosis is treated with isoniazid alone, approximately 70% of patients will develop isoniazid-resistant tuberculosis within a week to months. Therefore, all patients with the active form of tuberculosis must be treated with two or more antituberculosis drugs to prevent the development of drug resistance.

The anti-tuberculosis drugs available work through different mechanisms and at different places in the body. For example, isoniazid is most active at extracellular sites and has a pronounced effect on rapidly multiplying organisms. Rifampicin acts on both intracellular and extracellular sites, and can kill M.tuberculosis. Pyrazinamide acts in an acidic environment. Therefore, antituberculosis drugs can kill tuberculosis bacilli in different compartments in the body and at different growth rates.

Anti-tuberculosis drugs

Antituberculosis drugs are usually divided into several groups, based on their action against M.tuberculosis. Medications “ first lines “Used to treat non-resistant tuberculosis include isoniazid, rifampicin, ethambutol and pyrazinamide. These drugs are among the most potent and best tolerated antituberculosis drugs. When patients have drug-resistant tuberculosis, drugs called drugs are needed.” other traits “.

These drugs include fluoroquionlone, cycloserine, ethionamide or prothionamide, para-aminosalicylic acid, and several intravenous agents such as streptomycin, capreomycin, kanamycin, and amikacin. In patients with highly resistant tuberculosis, drugs are used “ third line “which are actually less potent, have more side effects, and are more expensive than first- and second-group drugs.

  • Isoniazid is one of the most potent antituberculosis drugs, and is effective in preventing drug resistance when given with another antituberculosis drug. Side effects include nausea and vomiting, skin rashes, inflammation of the liver (hepatitis) and neuropathy.
  • Rifampicin is also a potent antituberculosis drug that not only prevents the development of drug resistance when given with another drug, but also allows for shortening of administration. The typical duration of therapy for drug-resistant tuberculosis is six months, but if rifampicin is not used, the duration of therapy is extended to 12-18 months. Side effects include nausea and vomiting, diarrhea, skin rashes, hepatitis, flu-like symptoms, and discoloration of body fluids to an orange color, including tears, which can permanently stain soft contact lenses. Rifampicin is metabolized in the liver and interacts with many drugs, thus reducing the serum concentration of the drugs with which it interacts. Therefore, great care should be taken in identifying drugs that are administered concomitantly with rifampicin.
  • Ethambutol is a less potent drug than isoniazid or rifampicin, but it helps prevent drug resistance. Side effects include skin rashes, decreased visual acuity and red and green blindness (optic neuritis), and neuropathy. With doses currently administered, visual problems are rare.
  • Pyrazinamide, like rifampicin, allows a shorter duration of therapy. When pyrazinamide is not used, treatment is extended from six to nine months. Side effects include rash, joint pain and liver inflammation.

Drug administration

Patients with drug-resistant tuberculosis are treated with four drugs, which are given over a period of six months. These include first-line drugs, isoniazid, rifampicin, ethambutol, and pyrazinamide. After the first two months of therapy, pyrazinamide and ethambutol treatment is discontinued. Isoniazid and rifampicin are continued for another four months to complete the six-month therapy. Medications can be given daily, twice a week, or three times a week – with similar results. The expected outcome of treatment is excellent, as failure occurs in only 2-3% of cases.

Healthcare professionals usually give these medications under strict supervision. Directly observed therapy ensures that each drug is taken as prescribed, allowing for close monitoring of response to therapy, side effects, and toxicity. In some cases, patients take the therapy themselves, and we call this self-administered therapy.

Patients are closely monitored during therapy to ensure proper drug administration and to more easily monitor response to therapy and potential toxicity. Each drug has specific side effects and potential toxicity, as noted earlier. Three of the four antituberculosis drugs can cause inflammation of the liver (hepatitis), so patients are monitored for hepatitis by periodic blood tests.

Rifampicin causes body fluids to turn orange, which recedes when the drug is no longer used. Ethambutol can cause inflammation of the optic nerve, so regular assessments of visual abilities and green / red blindness tests are performed. Pyrazinamide often causes joint pain and can often cause gout attacks. Additionally, pyrazinamide can cause hepatitis.

Most patients with pulmonary tuberculosis will respond quickly to therapy with improvement in symptoms and eventual conversion of sputum cultures to a negative result. After two months of treatment, approximately 80% of patients with pulmonary tuberculosis will have a negative sputum culture result.


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