Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis). Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extrapulmonary TB may coexist with pulmonary TB.

General signs and symptoms include fever, chills, night sweats, loss of appetite, weight loss, and fatigue. Significant nail clubbing may also occur.

If a tuberculosis infection does become active, it most commonly involves the lungs (in about 90% of cases). Symptoms may include chest pain and a prolonged cough producing sputum. About 25% of people may not have any symptoms (i.e. they remain "asymptomatic"). Occasionally, people may cough up blood in small amounts, and in very rare cases, the infection may erode into the pulmonary artery or a Rasmussen's aneurysm, resulting in massive bleeding. Tuberculosis may become a chronic illness and cause extensive scarring in the upper lobes of the lungs. The upper lung lobes are more frequently affected by tuberculosis than the lower ones. The reason for this difference is not clear. It may be due to either better air flow, or poor lymph drainage within the upper lungs.

Patients with miliary tuberculosis often experience non-specific signs, such as coughing and enlarged lymph nodes. Miliary tuberculosis can also present with enlarged liver (40% of cases), enlarged spleen (15%), inflammation of the pancreas (<5%), and multiple organ dysfunction with adrenal insufficiency (adrenal glands do not produce enough steroid hormones to regulate organ function). Miliary tuberculosis may also present with unilateral or bilateral pneumothorax rarely. Stool may also be diarrheal in nature and appearance.

Other symptoms include fever, hypercalcemia, chorodial tubercles and cutaneous lesions.

Firstly, many patients can experience a fever lasting several weeks with daily spikes in morning temperatures.

Secondly, hypercalcemia prevails in 16 to 51% of tuberculosis cases. It is thought that hypercalcemia occurs as a response to increased macrophage activity in the body. Such that, 1,25 dihydroxycholecalciferol (also referred to as calcitriol) improves the ability of macrophages to kill bacteria; however, higher levels of calcitriol lead to higher calcium levels, and thus hypercalcemia in some cases. Thus, hypercalcemia proves to be an important symptom of miliary tuberculosis.

Thirdly, chorodial tubercules, pale lesions on the optic nerve, typically indicate miliary tuberculosis in children. These lesions may occur in one eye or both; the number of lesions varies between patients. Chorodial tubercules may serve as important symptoms of miliary tuberculosis, since their presence can often confirm suspected diagnosis.

Lastly, between 10 and 30% of adults, and 20–40% of children with miliary tuberculosis have tuberculosis meningitis. This relationship results from myobacteria from miliary tuberculosis spreading to the brain and the subarachnoid space; as a result, leading to tuberculosis meningitis.

The risk factors for contracting miliary tuberculosis are being in direct contact with a person who has it, living in unsanitary conditions, and having an unhealthy diet. In the U.S., risk factors for contracting the disease include homelessness and HIV/AIDS.

Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1–5 mm). Its name comes from a distinctive pattern seen on a chest radiograph of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds—thus the term "miliary" tuberculosis. Miliary TB may infect any number of organs, including the lungs, liver, and spleen. Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases.

Urogenital tuberculosis may cause strictures of the ureter, which, however, may heal when infection is treated.

A diagnosis of latent tuberculosis (LTB), also called latent tuberculosis infection (LTBI) means a patient is infected with "Mycobacterium tuberculosis", but the patient does not have active tuberculosis. Active tuberculosis can be contagious while latent tuberculosis is not, and it is therefore not possible to get TB from someone with latent tuberculosis. The main risk is that approximately 10% of these patients (5% in the first two years after infection and 0.1% per year thereafter) will go on to develop active tuberculosis. This is particularly true, and there is added risk, in particular situations such as medication that suppresses the immune system or advancing age.

The identification and treatment of people with latent TB is an important part of controlling this disease. Various treatment regimens are in use to treat latent tuberculosis, which generally need to be taken for several months.

The infection may affect the kidneys, ureter and bladder and may cause significant damage to each.

The co-epidemic of tuberculosis (TB) and human immunodeficiency virus (HIV) is one of the major global health challenges in the present time. The World Health Organization (WHO) reports 9.2 million new cases of TB in 2006 of whom 7.7% were HIV-infected. Tuberculosis is the most common contagious infection in HIV-Immunocompromised patients leading to death. These both diseases become dreadful in combination as HIV declines the human immunity while tuberculosis becomes progressive due to defective immune system.This condition becomes more severe in case of multi-drug (MDRTB) and extensively drug resistant TB (XDRTB), which are difficult to treat and contribute to increased mortality. See Multi-drug-resistant tuberculosis. Tuberculosis can occur at any stage of HIV infection. The risk and severity of tuberculosis increases soon after infection with HIV. A study on gold miners of South Africa revealed that the risk of TB was doubled during the first year after HIV seroconversion. Although tuberculosis can be a relatively early manifestation of HIV infection, it is important to note that the risk of tuberculosis progresses as the CD4 cell count decreases along with the progression of HIV infection. The risk of TB generally remains high in HIV-infected patients above the background risk of the general population even with effective immune reconstitution with ART maintaining high CD4 cell counts.

Extensively drug-resistant tuberculosis (XDR-TB) is a form of tuberculosis caused by bacteria that are resistant to some of the most effective anti-TB drugs. XDR-TB strains have arisen after the mismanagement of individuals with multidrug-resistant TB (MDR-TB).

Almost one in four people in the world is infected with TB bacteria. Only when the bacteria become active do people become ill with TB. Bacteria become active as a result of anything that can reduce the person’s immunity, such as HIV, advancing age, or some medical conditions. TB can usually be treated with a course of four standard, or first-line, anti-TB drugs (i.e., isoniazid, rifampin and any fluoroquinolone). If these drugs are misused or mismanaged, multidrug-resistant TB (MDR-TB) can develop. MDR-TB takes longer to treat with second-line drugs (i.e., amikacin, kanamycin, or capreomycin), which are more expensive and have more side-effects. XDR-TB can develop when these second-line drugs are also misused or mismanaged and therefore also become ineffective.

XDR-TB raises concerns of a future TB epidemic with restricted treatment options, and jeopardizes the major gains made in TB control and progress on reducing TB deaths among people living with HIV/AIDS. It is therefore vital that TB control be managed properly and new tools developed to prevent, treat and diagnose the disease.

The true scale of XDR-TB is unknown as many countries lack the necessary equipment and capacity to accurately diagnose it. It is estimated however that there are around 40,000 cases per year. As of June 2008, 49 countries had confirmed cases of XDR-TB. As of 2017, that number had risen to more than 100.

Vietnamese tuberculosis refers to certain forms of chronic melioidosis that look clinically very similar to tuberculosis. It is derived from the clinical appearance of the disease in American soldiers returning from the Vietnam War.

Totally drug-resistant tuberculosis (TDR-TB) is a generic term for tuberculosis strains that are resistant to a wider range of drugs than strains classified as extensively drug-resistant tuberculosis. TDR-TB has been identified in three countries; India, Iran, and Italy. The emergence of TDR-TB has been documented in four major publications. However, it is not yet recognised by the World Health Organization.

TDR-TB has resulted from further mutations within the bacterial genome to confer resistance, beyond those seen in XDR- and MDR-TB. Development of resistance is associated with poor management of cases. Drug resistance testing occurs in only 9% of TB cases worldwide. Without testing to determine drug resistance profiles, MDR- or XDR-TB patients may develop resistance to additional drugs. TDR-TB is relatively poorly documented, as many countries do not test patient samples against a broad enough range of drugs to diagnose such a comprehensive array of resistance. The United Nations' Special Programme for Research and Training in Tropical Diseases has set up a TDR Tuberculosis Specimen Bank to archive specimens of TDR-TB.

Multi-drug-resistant tuberculosis (MDR-TB) is a form of tuberculosis (TB) infection caused by bacteria that are resistant to treatment with at least two of the most powerful first-line anti-TB medications (drugs), isoniazid and rifampin. Some forms of TB are also resistant to second-line medications, and are called extensively drug-resistant TB (XDR-TB).

Tuberculosis is caused by infection with the bacteria Mycobacterium tuberculosis. Almost one in four people in the world are infected with TB bacteria. Only when the bacteria become active do people become ill with TB. Bacteria become active as a result of anything that can reduce the person’s immunity, such as HIV, advancing age, diabetes or other immunocompromising illnesses. TB can usually be treated with a course of four standard, or first-line, anti-TB drugs (i.e., isoniazid, rifampin and any fluoroquinolone).

However, beginning with the first antibiotic treatment for TB in 1943, some strains of the TB bacteria developed resistance to the standard drugs through genetic changes (see mechanisms.) Currently the majority of multidrug-resistant cases of TB are due to one strain of TB bacteria called the Beijing lineage. This process accelerates if incorrect or inadequate treatments are used, leading to the development and spread of multidrug-resistant TB (MDR-TB). Incorrect or inadequate treatment may be due to use of the wrong medications, use of only one medication (standard treatment is at least two drugs), not taking medication consistently or for the full treatment period (treatment is required for several months). Treatment of MDR-TB requires second-line drugs (i.e., fluoroquinolones, aminoglycosides, and others), which in general are less effective, more toxic and much more expensive than first-line drugs. Treatment schedules for MDR-TB involving fluoroquinolones and aminoglycosides can run for 2 years, compared to the 6 months of first-line drug treatment, and cost over $100,000 USD.If these second-line drugs are prescribed or taken incorrectly, further resistance can develop leading to XDR-TB.

Resistant strains of TB are already present in the population, so MDR-TB can be directly transmitted from an infected person to an uninfected person. In this case a previously untreated person develops a new case of MDR-TB. This is known as primary MDR-TB, and is responsible for up to 75% of cases. Acquired MDR-TB develops when a person with a non-resistant strain of TB is treated inadequately, resulting in the development of antibiotic resistance in the TB bacteria infecting them. These people can in turn infect other people with MDR-TB.

MDR-TB caused an estimated 480,000 new TB cases and 250,000 deaths in 2015. MDR-TB accounts for 3.3% of all new TB cases worldwide. Resistant forms of TB bacteria, either MDR-TB or rifampin-resistant TB, cause 3.9% of new TB cases and 21% of previously treated TB cases. Globally, most MDR-TB cases occur in South America, Southern Africa, India, China, and the former Soviet Union.

Treatment of MDR-TB requires treatment with second-line drugs, usually four or more anti-TB drugs for a minimum of 6 months, and possibly extending for 18–24 months if rifampin resistance has been identified in the specific strain of TB with which the patient has been infected. Under ideal program conditions, MDR-TB cure rates can approach 70%.

Symptoms of XDR-TB are no different from ordinary or drug-susceptible TB: a cough with thick, cloudy mucus (or sputum), sometimes with blood, for more than 2 weeks; fever, chills, and night sweats; fatigue and muscle weakness; weight loss; and in some cases shortness of breath and chest pain. A person with these symptoms does not necessarily have XDR-TB, but they should see a physician for diagnosis and a treatment plan. TB patients whose symptoms do not improve after a few weeks of treatment for TB and are taking treatment should inform their clinician or nurse.

Fever and headache are the cardinal features, confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits.

Some people with bronchiectasis may have a cough productive of frequent green/yellow mucus (sputum), up to 240 ml (8 oz) daily. Bronchiectasis may also present with coughing up blood (hemoptysis) in the absence of sputum, called "dry bronchiectasis". Sputum production may also occur without coloration. People with bronchiectasis may have bad breath indicative of active infection. Frequent bronchial infections and breathlessness are two possible indicators of bronchiectasis.

Crepitations and expiratory rhonchi may be heard on auscultation. Nail clubbing is rare.

Primary inoculation tuberculosis (also known as "Cutaneous primary complex," "Primary tuberculous complex," and "Tuberculous chancre") is a skin condition that develops at the site of inoculation of tubercle bacilli into a tuberculosis-free individual.

A Simon focus is a tuberculosis (TB) nodule that can form in the apex of the lung when a primary TB infection elsewhere in the body spreads to the lung apex via the bloodstream. Simon focus nodules are often calcified.

The initial lesion is usually a small focus of consolidation, less than 2cm in diameter and located within 1 to 2 cm of the apical pleura. In adolescence, Simon foci may become reactivated and develop into Assmann foci. Such foci are sharply circumscribed, firm, gray-white to yellow areas that have a variable amount of central caseation and peripheral fibrosis.

A study conducted on 452 patients revealed that the genotype responsible for higher IL-10 expression makes HIV infected people more susceptible to tuberculosis infection. Another study on HIV-TB co-infected patients also concluded that higher level of IL-10 and IL-22 makes TB patient more susceptible to Immune reconstitution inflammatory syndrome (IRIS). It is also seen that HIV co-infection with tuberculosis also reduces concentration of immunopathogenic matrix metalloproteinase (MMPs) leading to reduced inflammatory immunopathology.

Because the TVC's entry point usually is the site of a trauma, wound or puncture in the skin (during an autopsy, for example), the most frequent site for the wart are the hands. But it can occur anywhere in the skin, such as in the sole of the feet, in the anus, and, in the case of children from developing countries, in the buttocks and knees. This is because children from countries of high incidence of tuberculosis can contract the lesion after contact with tuberculous sputum, by walking barefoot, sitting or playing on the ground.

When recent, the skin lesion has the outside appearance of a wart or verruca, thus it can be confused with other kinds of warts. It evolves to an annular red-brown plaque with time, with central healing and gradual expansion in the periphery. In this phase, it can be confused with fungal infections such as blastomycosis and chromoblastomycosis.

A Ghon focus is a primary lesion usually subpleural, often in the mid to lower zones, caused by "Mycobacterium bacilli" (tuberculosis) developed in the lung of a nonimmune host (usually a child). It is named for Anton Ghon (1866–1936), an Austrian pathologist.

It is a small area of granulomatous inflammation, only detectable by chest X-ray if it calcifies or grows substantially (see tuberculosis radiology). Typically these will heal, but in some cases, especially in immunosuppressed patients, it will progress to miliary tuberculosis (so named due to the granulomas resembling millet seeds on a chest X-ray).

The classical location for primary infection is surrounding the lobar fissures, either in the upper part of the lower lobe or lower part of the upper lobe.

If the Ghon focus also involves infection of adjacent lymphatics and hilar lymph nodes, it is known as the Ghon's complex or primary complex. When a Ghon's complex undergoes fibrosis and calcification it is called a Ranke complex.

Bronchiectasis has both congenital and acquired causes, with the latter more frequent. Cystic fibrosis is a cause in up to half of cases. The cause in 10-50% of those without cystic fibrosis is unknown; bronchiectasis without CF is known as non-CF bronchiectasis (NCBE).

As the histologic and clinical indications, as well as tumor markers such as the CA-125, are similar, it is often difficult to differentiate tuberculoma from cancer. For these reasons, tuberculosis should always be considered in the differential diagnosis of cancer.

With the passage of time " Mycobacterium tuberculosis" (also called" Bacillus Koch") can transform into crystals of calcium. These can affect any organ such as the brain, intestine, ovaries, breast, lungs, esophagus, intestine, liver, pancreas, bones, and many others.

Tuberculous meningitis is also known as TB meningitis or tubercular meningitis. Tuberculous meningitis is "Mycobacterium tuberculosis" infection of the meninges—the system of membranes which envelop the central nervous system.

Tuberculosis verrucosa cutis (also known as "lupus verrucosus", "prosector's wart", and "warty tuberculosis") is a rash of small, red papular nodules in the skin that may appear 2–4 weeks after inoculation by "Mycobacterium tuberculosis" in a previously infected and immunocompetent individual.

It is so called because it was a common occupational disease of prosectors, the preparers of dissections and autopsies. Reinfection by tuberculosis via the skin, therefore, can result from accidental exposure to human tuberculous tissue in physicians, pathologists and laboratory workers; or to tissues of other infected animals, in veterinarians, butchers, etc. Other names given to this form of skin tuberculosis are anatomist's wart and verruca necrogenica (literally, generated by corpses).

TVC is one of the many forms of cutaneous tuberculosis, such as the tuberculous chancre (which results from the inoculation in people without immunity), and the reactivation cutaneous tuberculosis (the most common form, which appears in previously infected patients). Other forms of cutaneous tuberculosis are: lupus vulgaris, scrofuloderma, lichen scrofulosorum, erythema induratum and the papulonecrotic tuberculid.

It was described by René Laennec in 1826.