Tuberculosis, MTB, or TB (short for tubercle bacillus), in the past also called phthisis, phthisis pulmonalis, or consumption, is a widespread, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis. Tuberculosis typically attacks the lungs, but can also affect other parts of the body. It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air. Most infections do not have symptoms, known as latent tuberculosis. About one in ten latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those so infected.

Means of spread 

It is spread through the air when people who have an active TB infection cough, sneeze, or otherwise transmit respiratory fluids through the air.[2] The principal entry into the body is by inhalation, though the disease can be contracted from milk and other dairy products taken from infected cattle. In rare cases it can also be transmitted via infected urine. Frequent exposure to victims substantially increases the risk of infection. If not revealed to sunlight, the bacillus can survive for months in dried sputum, and is able to multiply in damp, dark environments.

Effects on the human body 
There are two stages to the disease.
Tuberculosis typically attacks the lungs, but can also affect other parts of the body. The classic symptoms of active TB infection are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss (the last of these giving rise to the formerly common term for the disease, "consumption"). Infection of other organs causes a wide range of symptoms. Most infections do not have symptoms, known as latent tuberculosis. About one in ten latent infections eventually progresses to active disease which, if left untreated, kills more than 50% of those so infected.

Primary infection 

This initial stage often occurs in childhood. The bacillus reaches the middle and lower lung areas to gain access to the bloodstream. It subsequently lodges in any organ. Childhood symptoms are often lethargy, poor appetite, loss of weight, and fever. Although the disease is normally contained, the body does not rid itself of the bacillus – instead the disease is said to become quiescent, or dormant. No immunity is developed.
In certain cases, the bacillus enters the bone structure, especially that of the spinal column, to produce later deformities such as a hunched back or ‘spidery’ legs. This course is known as Pott’s Disease. Male children are more prone to Pott’s Disease than are female.

Secondary infection 

If the individual is re-infected or if the body defenses are lowered through malnourishment, injury, attack from another disease, or – in females – as a result of childbirth, tuberculosis can enter its secondary, or chronic, stage. This may emerge several decades after the primary infection and usually takes place in a particular part of the body.

By far the most common form of the disease is pulmonary tuberculosis. The first symptoms can be slight: a listlessness and a vague pain in the chest; but the situation worsens to cause a sharper pain, shallow breathing, chills, fever, and an acute and exhausting cough accompanied by a spitting of blood.
A frequent consequence of pulmonary tuberculosis is inflammation of the airtight membrane that surrounds the lungs. The cavity that contain the lungs is maintained in a healthy individual at less than atmospheric pressure in order for the lung to operate correctly. In a tuberculosed person the airtight membrane can eventually be perforated by the bacillus, causing a sudden collapse of the lung.

Another possibility is the development of broncho-pneumonic tuberculosis, wherein the linings of the bronchial tubes are rapidly destroyed. This usually fatal course was at one time known as ‘galloping consumption’.

With tuberculosis, it is not the bacillus itself that causes the harm – for instance, it does not release any toxic material. Instead, the body responds to the micro-organisms in the normal way by killing them, but rather than the debris being cleared from the site it steadily builds up a deposit to form ‘cheesy’ (or caseous) tubercles. It is the tubercles that cause the inflammation and destruction.

Moreover, wherever the bacillus might be lodged in the body, its requirements cause a vitamin deficiency in the human host. The situation can be exacerbated by a loss of appetite for food. In short, the body is not able to repair itself adequately and becomes ‘consumptive’.
History
Tuberculosis has been present in humans since antiquity.[9] The earliest unambiguous detection of M. tuberculosis involves evidence of the disease in the remains of bison in Wyoming dated to around 17,000 years ago.[102] However, whether tuberculosis originated in bovines, then was transferred to humans, or whether it diverged from a common ancestor, is currently unclear.[103] A comparison of the genes of M. tuberculosis complex (MTBC) in humans to MTBC in animals suggests humans did not acquire MTBC from animals during animal domestication, as was previously believed. Both strains of the tuberculosis bacteria share a common ancestor, which could have infected humans as early as the Neolithic Revolution.[104]

Skeletal remains show prehistoric humans (4000 BC) had TB, and researchers have found tubercular decay in the spines of Egyptian mummies dating from 3000–2400 BC.[105] Genetic studies suggest TB was present in the Americas from about 100 AD.[106]

Phthisis is a Greek word for consumption, an old term for pulmonary tuberculosis;[107] around 460 BC, Hippocrates identified phthisis as the most widespread disease of the times. It was said to involve fever and the coughing up of blood, which was almost always fatal.[108]

Before the Industrial Revolution, folklore often associated tuberculosis with vampires. When one member of a family died from it, the other infected members would lose their health slowly. People believed this was caused by the original person with TB draining the life from the other family members.[109]
Although the pulmonary form associated with tubercles was established as a pathology by Dr Richard Morton in 1689,[110][111] due to the variety of its symptoms, TB was not identified as a single disease until the 1820s. It was not named "tuberculosis" until 1839, by J. L. Schönlein.[112]

During 1838–1845, Dr. John Croghan, the owner of Mammoth Cave, brought a number of people with tuberculosis into the cave in the hope of curing the disease with the constant temperature and purity of the cave air; they died within a year.[113] Hermann Brehmer opened the first TB sanatorium in 1859 in Görbersdorf (now Sokołowsko), Silesia.[114]

The bacillus causing tuberculosis, M. tuberculosis, was identified and described on 24 March 1882 by Robert Koch. He received the Nobel Prize in physiology or medicine in 1905 for this discovery.[115] Koch did not believe the bovine (cattle) and human tuberculosis diseases were similar, which delayed the recognition of infected milk as a source of infection. Later, the risk of transmission from this source was dramatically reduced by the invention of the pasteurization process. Koch announced a glycerine extract of the tubercle bacilli as a "remedy" for tuberculosis in 1890, calling it "tuberculin". While it was not effective, it was later successfully adapted as a screening test for the presence of pre-symptomatic tuberculosis.[116]

Albert Calmette and Camille Guérin achieved the first genuine success in immunization against tuberculosis in 1906, using attenuated bovine-strain tuberculosis. It was called bacille Calmette–Guérin (BCG). The BCG vaccine was first used on humans in 1921 in France,[117] but received widespread acceptance in the US, Great Britain, and Germany only after World War II.[118]

Tuberculosis caused the most widespread public concern in the 19th and early 20th centuries as an endemic disease of the urban poor. In 1815, one in four deaths in England was due to "consumption". By 1918, one in six deaths in France was still caused by TB. After TB was determined to be contagious, in the 1880s, it was put on a notifiable disease list in Britain; campaigns were started to stop people from spitting in public places, and the infected poor were "encouraged" to enter sanatoria that resembled prisons (the sanatoria for the middle and upper classes offered excellent care and constant medical attention).[114] Whatever the (purported) benefits of the "fresh air" and labor in the sanatoria, even under the best conditions, 50% of those who entered died within five years (circa 1916).[114]

In Europe, rates of tuberculosis began to rise in the early 1600s to a peak level in the 1800s, when it caused nearly 25% of all deaths.[119] By the 1950s, mortality had decreased nearly 90%.[120] Improvements in public health began significantly reducing rates of tuberculosis even before the arrival of streptomycin and other antibiotics, although the disease remained a significant threat to public health such that when the Medical Research Council was formed in Britain in 1913, its initial focus was tuberculosis research.[121]

In 1946, the development of the antibiotic streptomycin made effective treatment and cure of TB a reality. Prior to the introduction of this drug, the only treatment (except sanatoria) was surgical intervention, including the "pneumothorax technique", which involved collapsing an infected lung to "rest" it and allow tuberculous lesions to heal.[122]

Because of the emergence of MDR-TB, surgery has been re-introduced as an option within the generally accepted standard of care in treating TB infections. Current surgical interventions involve removal of pathological chest cavities ("bullae") in the lungs to reduce the number of bacteria and to increase the exposure of the remaining bacteria to drugs in the bloodstream, thereby simultaneously reducing the total bacterial load and increasing the effectiveness of systemic antibiotic therapy.[123]

Hopes of completely eliminating TB (cf. smallpox) from the population were dashed after the rise of drug-resistant strains in the 1980s. The subsequent resurgence of tuberculosis resulted in the declaration of a global health emergency by the World Health Organization in 1993.[124]

Notable people who died of tuberculosis

1. Wikipedia; Category:Deaths from tuberculosis.
2. Famous People Who Died of Tuberculosis (702 people listed)

• Eleanor Roosevelt, wife of President Franklin D Roosevelt (1884-1962)
• Vivien Leigh, actress (1913-1967)
• Frederic Chopin, pianist, composer (1810-1849)
• Andrew Jackson, 7th President of the US (1767-1845)
• George Orwell, English author (1903-1950)
• Franz Kafka, German-language writer (1883-1924)
• Henry David Thoreau, American author (1817-1862)
• Denholm Elliott, English actor (1922-1992)
• Karol Szymanowski, Polish composer & pianist (1882-1937)
• Jane Austen, English novelist (1775-1817)
• Charles IX, King of France 1560-till death (1550-1574)
• Armand Jean du Plessis, Cardinal of Richelieu, French noble & statesman (1585-1642)
• Helene Costello, American stage & film actress during silent era (1906-1957)
• Barbara La Marr, American stage & film actress (1896-1926)
• Wallace Thurman, American novelist (1902-1934)
• Manuel L. Quezon, 2nd President of the Philippines (1878-1944)
• Marcelo H. del Pilar, Filipino writer, lawyer, journalist, and freemason (1850-1896)
• Simón Bolívar, Venezuelan military and political leader (1783-1830)

External links

• Wikipedia; Category:Deaths from tuberculosis.
• Ranker.com's Featured Lists; Famous People Who Died of Tuberculosis
• Infectious Diseases in History, by Brian Williams BA (Hons) in 1997
• Wikipedia - Tuberculosis

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