Details, Explanation and Meaning About Tuberculosis

Tuberculosis Guide, Meaning , Facts, Information and Description

Tuberculosis is also called TB, consumption (TB seemed to consume people from within with its symptoms of bloody cough, fever, pallor, and long relentless wasting), wasting disease, White Plague (TB sufferers appeared markedly pale), phthisis (Greek for consumption), and phthisis pulmonalis. Other names are scrofula (swollen neck glands) or King's Evil (so called because it was believed that a king's touch would heal scrofula), Pott's disease of the spine, and miliary TB (x-ray lesions look like millet seeds).

TB disease is an infection which most commonly affects the lungs, where it is called pulmonary TB. But it can also affect the central nervous system (meningitis), lymphatic system, circulatory system (miliary TB), genitourinary system, and bones and joints.

TB is caused by the bacterium Mycobacterium tuberculosis. It is the most common major infectious disease today, infecting two billion people or one-third of the world's population, with nine million new cases of active disease annually, resulting in two million deaths, mostly in developing countries.

Most of those infected (90 percent) have asymptomatic latent TB infection (LTBI). There is a 10 percent lifetime chance that it may progress to active TB disease in which, if left untreated, more than 50 percent of people will die. It is one of the top three infectious disease killers in the world: HIV/AIDS kills 3 million people each year, TB kills 2 million, and malaria kills 1 million.

The neglect of TB control programs, HIV/AIDS, and immigration has caused a resurgence of tuberculosis. Multiple drug resistant strains of MDR-TB is increasing. The World Health Organization declared TB a global health emergency in 1993.

Table of contents
1 The bacterium
2 The disease
3 Diagnosis
4 Treatment
5 Prevention
6 History
7 Tuberculosis in art and literature
8 See also
9 References
10 External links

The bacterium

''.]] The cause of tuberculosis, Mycobacterium tuberculosis (MTB), is a slow-growing Gram-positive aerobic bacterium that divides every 16 to 20 hours. This is extremely slow compared to other bacteria which tend to have division times measured in minutes (among the fastest growing bacteria is a strain of E. coli that can divide roughly every 20 minutes). It is a small rod-like bacillus which can withstand weak disinfectants and can survive in a dry state for weeks but, spontaneously, can only grow within a host organism (in vitro culture of M. tuberculosis took a long time to be achieved, but is nowadays a normal laboratory procedure).

MTB is identified microscopically by its staining characteristics: it retains certain stains after being treated with acidic solution, and is thus classified as an "acid-fast bacillus" or "AFB". In the most common staining technique, the Ziehl-Neelsen stain, AFB are stained a bright red which stands out clearly against a blue background. Acid-fast bacilli can also be visualized by fluorescent microscopy, and by auramine-rhodamine stain.

The M. tuberculosis complex includes 3 other mycobacteria which can cause tuberculosis: M. bovis, M. africanum, and M. microti. The first two are very rare causes of disease and the last one does not cause human disease.

Nontuberculous mycobacteria (NTM) are other mycobacteria (besides M. leprae which causes leprosy) which may cause pulmonary disease resembling TB, lymphadenitis, skin disease, or disseminated disease. These include Mycobacterium avium, M. kansasii, and others.

The disease

Transmission

TB is spread through air droplets which are expelled when persons with infectious TB disease cough, sneeze, speak, or sing. Close contacts (persons with prolonged, frequent, or intense contact) are at highest risk of becoming infected (22 percent infection rate). Others at risk include foreign-born from areas where TB is common, residents and employees of high-risk congregate settings, health care workers who serve high-risk clients, medically underserved, low-income populations, high-risk racial or ethnic minority populations, children exposed to adults in high-risk categories, and persons who inject illicit drugs.

Transmission occurs only from persons with active TB disease (not latent TB infection).

The probability of transmission depends upon: infectiousness of the person with TB (quantity expelled), environment of exposure, duration of exposure, and virulence of the organism.

The chain of transmission can be stopped by isolating patients with active disease and starting effective anti-tuberculous therapy.

Pathogenesis

While only 10 percent of TB infection progresses to TB disease, if untreated the death rate is 50 percent.

Infection

TB infection begins when TB bacilli reach the pulmonary alveoli, from which they may spread to local lymph nodes, and then through the bloodstream to the more distant tissues and organs where TB disease is likely to develop: lung apices, kidneys, brain, and bone.

The bacterium causes a type IV immune hypersensitivity response. T-lymphocyts secrete cytokines and recruit and activate macrophages. These macrophages form spherical aggregates in the tissues called granulomas. A granuloma when viewed under the microscope by histology shows a central zone of large macrophagic cells surrounded by a zone of T-lymphocytes. Some of the macrophages fuse to form multinucleate giant cells termed Langerhans Giant cells. Tuberculosis is therefore classed as one of the granulomatous inflammatory conditions.

The granullomas in tuberculosis are called tubercles, or tuberculous nodules. They can be seen in tissues by the naked eye as small white spots 1-2mm in size.

This type IV immune response can kill some bacteria. Bacteria can also survive where they live within the macrophagic cells. If the affected patient has a strong immune system and is well nourished, it is likely that the immune response will eliminate bacteria and the tubercle heals by formation of a scar. Usually the immune system is able to halt the multiplication of TB bacilli, preventing further spread in about 90 percent of cases. However if a person has a weak immune system or is poorly nourished bacteria are not eliminated and proliferate. The tubercles enlarge and there is local tissue destruction.

Another feature of the granulomas of tuberculosis is the development of cell death, also called necrosis, in the centre of tubercles. To the naked eye this has the texture of soft white cheese and was termed caseous necrosis.

If TB bacteria gain entry to the blood stream from an area of tissue damage they spread through the body and set up myriad foci of infection, all appearing as tiny white tubercles in the tissues. This is called miliary tuberculosis and has a high case fatality.

In many patients the infection waxes and wanes. Tissue destruction and necrosis are balanced by healing and fibrosis. Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material. In the lung some of these cavities are in continuity with the air passages bronchi. This material may therefore be coughed up. It contains living bacteria and can pass on infection.

treatment with appropriate antibiotics kills bacteria and allows healing to take place. Affected areas are eventually replaced by scar tissue.

Disease

In those people in whom TB bacilli overcome the immune system defenses and begin to multiply, there is progression from TB infection to TB disease. This may occur soon after infection (primary TB disease – 1 to 5 percent) or many years after infection (post primary TB, secondary TB, reactivation TB disease of dormant bacilli – 5 to 9 percent).

About five percent of infected persons will develop TB disease in the first two years, and another five percent will develop disease later in life. In all, about 10 percent of infected persons with normal immune systems will develop TB disease in their lifetime.

Some medical conditions increase the risk of progression to TB disease. In HIV infected persons with TB infection, the risk increases to 10 percent each year instead of 10 percent over a lifetime. Other such conditions include drug injection, substance abuse, recent TB infection (within two years) or history of inadequately treated TB, chest X-ray suggestive of previous TB (fibrotic lesions and nodules), diabetes mellitus, silicosis, prolonged corticosteroid therapy and other immunosuppressive therapy, head and neck cancers, hematologic and reticuloendothelial diseases (leukemia and Hodgkin's disease), end-stage renal disease, intestinal bypass or gastrectomy, chronic malabsorption syndromes, or low body weight (10 percent or more below the ideal).

Some drugs, including rheumatoid arthritis drugs that work by blocking tumor necrosis factor (an inflammation-causing protein), may raise the risk of contracting tuberculosis or causing a latent infection to become active.

TB disease most commonly affects the lungs (75 percent or more), where it is called pulmonary TB. Symptoms include a productive, prolonged cough of more than three weeks duration, chest pain, and hemoptysis. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, and easy fatigability. The term consumption arose because sufferers appeared as if they were "consumed" from within by the disease.

Extrapulmonary sites include the pleura, central nervous system (meningitis), lymphatic system (scrofula of the neck), genitourinary system, and bones and joints (Pott's disease of the spine). An especially serious form is "disseminated", or "miliary" TB, so named because the lung lesions so-formed resemble millet seeds on x-ray. These are more common in immunosuppressed persons and in young children. Pulmonary TB may co-exist with extrapulmonary TB.

Drug resistance

Drug-resistant TB is transmitted in the same way as drug-susceptible TB. Primary resistance develops in persons initially infected with resistant organisms. Secondary resistance (acquired resistance) develops during TB therapy due to inadequate treatment regimen or not taking the prescribed regimen appropriately.

Diagnosis

A complete medical evaluation for TB includes a medical history, a physical examination, a tuberculin skin test, a chest X-ray, and microbiologic smears and cultures.

Medical history

The medical history includes obtaining the symptoms of pulmonary TB: productive, prolonged cough of three or more weeks, chest pain, and hemoptysis. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, and easy fatigability. Other parts of the medical history include prior TB exposure, infection or disease; past TB treatment; demographic risk factors for TB; and medical conditions that increase risk for TB disease such as HIV infection.

Tuberculosis should be suspected when a persistent respiratory illness in an otherwise healthy individual does not respond to regular antibiotics.

Physical examination

A physical examination is done to assess the patient's general health and find other factors which may affect the TB treatment plan. It cannot be used to confirm or rule out TB.

Chest X-ray

like this one in the patient's right upper lobe.]]

In active pulmonary TB, infiltrates or consolidations and/or cavities are often seen in the upper lungss with or without mediastinal or hilar lymphadenopathy. However, lesions may appear anywhere in the lungs. In HIV and other immunosuppresseded persons, any abnormality may indicate TB or the chest X-ray may even appear entirely normal.

Abnormalities on chest radiographs may be suggestive of, but are never diagnostic of, TB. However, chest radiographs may be used to rule out the possibility of pulmonary TB in a person who has a positive reaction to the tuberculin skin test and no symptoms of disease.

See Tuberculosis radiology for more information.

Laboratory

QuantiFERON-TB is a blood test that measures the patient’s immune reactivity to the TB bacteria and is useful for initial and serial testing of persons with an increased risk of latent tuberculosis infection (LTBI). It is not useful in active TB disease. A fact sheet from CDC is available.

Microbiological studies '' form in this culture.]] Sputum smears and cultures should be done for acid-fast bacilli if the patient is producing sputum. If no sputum is being produced, a laryngeal swab, bronchoscopy or fine needle aspiration should be considered. Other mycobacteria are also AFB. Further PCR or gene probe tests can distinguish M. tuberculosis from other mycobacteria. If this is not available, a culture of the AFB can distinguish the various forms of mycobacteria, although results from this may take four to eight weeks for a conclusive answer.

Tuberculin skin test

Two tests are available: the Mantoux and Heaf tests.

Mantoux skin test

for TB involves intradermally injecting PPD tuberculin and measuring the size of induration 48-72 hours later.]]

The Mantoux skin test is used in the United States and is endorsed by the American Thoracic Society and Centers for Disease Control and Prevention (CDC). Multiple puncture tests such as the Tine test are not recommended.

For information about the test including reading, false positive and false negative results, anergy testing, two-step testing and future developments, see Mantoux skin test.

If a person has had a history of a positive tuberculin skin test, another skin test is not needed.

Heaf test

The Heaf test is used in the United Kingdom and is endorsed by the British Thoracic Society.

The equivalent Mantoux test positive levels done with 10 TU (0.1 ml 100 TU/ml, 1:1000) are

  • 0-4 mm induration (Heaf 0-1)
  • 5-14 mm induration (Heaf 2)
  • >15 mm induration (Heaf 3-4)

Classification of tuberculin reaction

An induration (palpable raised hardened area of skin) of more than 5-15 mm (depending upon the person's risk factors) to 10 Mantoux units is considered a positive result, indicating TB infection.

A tuberculin test conversion is defined as an increase of 10 or more mm within a 2-year period regardless of age.

Contact screening

When someone is diagnosed with tuberculosis, all their close contacts should be screened for TB with a tuberculin skin test or a chest x-ray or both.

Tuberculosis classification system

The current clinical classification system for TB (Class 0 to 5) is based on the pathogenesis of the disease.

The U.S. Citizenship and Immigration Services has an additional TB classification (Class A, B1, or B2) for immigrants and refugees developed by the Centers for Disease Control and Prevention (CDC). The (Class) B notification program is an important screening strategy to identify new arrivals who have a high risk for TB.

See Tuberculosis classification for more details.

Treatment

Persons with TB infection (class 2 or class 4 TB), but who do not have TB disease (class 3 or class 5 TB), cannot spread the infection to other people. TB infection in a person who does not have TB disease is not considered a case of TB and is often referred to as latent TB infection (LTBI). This distinction is important because treatment options will be different for a person who has LTBI instead of active TB disease.

Treatment of latent TB infection

Treatment of latent TB infection (LTBI) is essential to controlling and eliminating TB by reducing the risk that TB infection will progress to disease.

Although the terms "preventive therapy" and "chemoprophylaxis" have been used for decades, they have also been confusing because it rarely results in true primary prevention of infection as with vaccinations. The terminology "treatment of LTBI" will hopefully promote greater understanding of the concept for both patients and providers, resulting in more widespread implementation of this essential TB control strategy.

Assessment to rule out active TB is necessary before treatment for LTBI is started.

Candidates for treatment of LTBI are those very high-risk groups with positive tuberculin of 5 mm or more as well as those high-risk groups with skin test 10 mm or more. See classification of tuberculin reaction.

There are several treatment regimens available:

Isoniazid (INH) for 9 months (270 daily doses taken within 12 months) is the optimal regimen. (93% effective)

  • Isoniazid for 6 months (180 daily doses within 9 months) might be adopted by a local TB program based on cost-effectiveness and patient compliance. The shorter regimen is not recommended for children or persons with radiographic evidence of prior tuberculosis (old fibrotic lesions). (69% effective)

    A twice-weekly regimen for the above 2 treatment regimens is an alternative if administered under Directly observed therapy (DOT).

  • Rifamin only for 4-months (120 daily doses within 6 months) is an alternative for those who are unable to take isoniazid or pyrazinamide.

    Rifampin and pyrazinamide is no longer recommended for treatment of LTBI (but is still useful in active TB). (See References Updates).

  • Treatment Regimen Chart adopted from Table 10 of Targeted Tuberculin Testing and Treatment of Latent Tuberculosis Infection (see References)

    Since about 10 percent of latent TB infection progresses to active TB disease, the 9 month INH treatment regimen reduces the 10 percent risk to less than 1 percent while the 6 month INH treatment reduces it to 3 percent. Treatment is recommended to prevent infecting others and reducing death rates (50 percent if untreated). Currently TB disease kills 2 million people each year mostly in developing countries

    Close contacts

    Close contacts are those sharing the same household or other enclosed environments. Those most at risk are children under 4 years of age, immunosuppressed people, and others who may develop TB disease quickly after infection. Close contacts who have had a negative tuberculin skin test reaction (less than 5 mm of induration) should be retested 10 to 12 weeks after they were last exposed to TB. Treatment of LTBI may be discontinued if the skin test result is again negative and if the person is no longer exposed to TB. However, immunosuppressed persons, including those with HIV disease, should complete the course of LTBI treatment regardless of the skin test reaction.

    Children and adolescents

    Children less than 4 years of age are at greater risk of having their infection progress to disease and to develop life-threatening forms of TB. These close contacts should receive treatment for LTBI even if the tuberculin skin test and chest X-ray do not suggest TB, because infected infants may be anergic as late as 6 months of age.

    A second tuberculin test should be placed 10 to 12 weeks after the last exposure to infectious TB. Treatment can be discontinued if it is also negative.

    Treatment of active TB disease

    The current accepted first-line therapy is a combination of the drugs rifampicin, isoniazid (INH), pyrizinamide, and ethambutol. After two months, the number of drugs is reduced. A typical treatment for a standard (i.e. non-drug resistant) strain of TB is 2HRZE / 4HR (= two months of INH, Rifampin, Pyrazinmid and Ethambutol followed by four months of Rifampin and INH). The number of relapses is about 2-3% this way. Medication can be given two or three times per week (different/higher dosages) with the same results as daily therapy.

    Why four drugs? If only one drug is given, what ends up happening is that all the bacteria sensitive to that drug are killed and three months later, the patient will be infected with progeny of the bacteria that were resistant to that particular drug. Rifampicin and isoniazid are bactericidal agents that kill the bacteria, pyrizinamide acts well against the intracellular bacteria which are dormant inside macrophages and other cells, and ethambutol is a bacteriostatic agent that inhibits bacterial proliferation while the other drugs kill off the TB. Rifampin is the drug that gives the best "sterilization"; this means that it will kill dormant bacteria very well in order to lower the number of relapses after a successful treatment.

    Streptomycin is used if the initial 4-drug therapy fails, often in conjunction with other second-line drugs such as capreomycin, cycloserine, new macrolides, quinolones, and protionamide. Streptomycin and capreomycin are not available as oral medications and must be injected. The newer linezolid (of the oxazolidinone class) has anti-mycobacterial activity in the laboratory, and is a promising drug to be evaluated in combination with others, either for those persons with intolerance to usual drugs, or for TB resistance to usual combinations.

    Treatment monitoring

    At least monthly, patients should be evaluated for adherence to the prescribed regimen, signs and symptoms of active TB disease or hepatitis.

    Patients with TB disease should be monitored monthly until cultures convert to negative. After 3 months of medications, if cultures are positive or symptoms do not resolve, reevaluate for potential drug-resistant disease or nonadherence to drug regimen. If cultures do not convert to negative dispite 3 months of therapy, consider initiating DOT.

    DOTS or Directly Observed Treatment, Short-course is currently recommended by the World Health Organization (WHO). The mainstay of this is the DOT or Directly Observed Treatment portion which involves health care workers directly monitoring tuberculosis patients actually swallowing their anti-tuberculous therapy for at least the first two months of treatment. Treatment with properly implemented DOTS has a success rate exceeding 95% and prevents the emergence of further multi-drug resistant strains of tuberculosis.

    Adverse drug reactions are expected in 20-25% of patients but only 5% of all patients will have a severe enough reaction to warrant a change in their drug regimen. Hepatic damage is the most significant of the drug reactions. Patients should immediately report any adverse reactions.

    Baseline lab testing is not routinely indicated for all patients. Baseline liver function tests are indicated if there are risks for liver disease or if patient has HIV infection, or pregnant.

    Peripheral neuropathy and CNS effects are associated with the use of isoniazid and is due to pyridoxine (vitamin B6) depletion, but is uncommon at doses of 5 mg/kg. Persons with conditions in which neuropathy is common (e.g., diabetes, uremia, alcoholism, malnutrition, HIV-infection), as well as pregnant women and persons with a seizure disorder, may be given pyridoxine (vitamin B6) (10-50 mg/day) with isoniazid.

    In busy clinics, because pyridoxine is inexpensive and relatively harmless, it is commonly given as a supplement to all patients to save time in verifying if a patient is at risk for neuropathy.

    Prevention

    Prevention and control efforts include three priority strategies:
    • identifying and treating all persons who have TB disease
    • finding and evaluating persons who have been in contact with TB patients to determine whether they have TB infection or disease, and treating them appropriately, and
    • testing high-risk groups for TB infection to identify candidates for treatment of latent infection and to ensure the completion of treatment.

    In tropical areas where the incidence of atypical mycobacteria is high, exposure to
    nontuberculous mycobacteria gives some protection against TB.

    BCG vaccine

    Many countries use BCG vaccine as part of their TB control programs, especially for infants. The protective efficacy of BCG for preventing serious forms of TB (e.g. meningitis) in children is high (greater than 80 percent). However, the protective efficacy for preventing pulmonary TB in adolescents and adults is variable, from 0 to 80 percent. In the United Kingdom, children aged 10-14 are typically immunized during school.

    The effectiveness of BCG is much lower than in areas where mycobacteria are much less prevalent. In the USA, BCG vaccine is not routinely recommended except for selected persons who meet specific criteria:

    • Infants or children with negative skin-test result who are continually exposed to untreated or ineffectively treated patient or will be continually exposed to multidrug-resistant TB.
    • Healthcare workers considered on individual basis in settings in which high percentage of MDR-TB patients has been found, transmission of MDR-TB are likely, and TB control precautions have been implemented and not successful.

    BCG vaccine and tuberculin skin test

    Tuberculin skin testing is not contraindicated for BCG-vaccinated persons.

    Latent TB infection (LTBI) diagnosis and treatment for LTBI is considered for any BCG-vaccinated person whose skin test is 10 mm or greater, if any of these circumstances are present:

    • Was contact of another person with infectious TB
    • Was born or has resided in a high TB prevalence country
    • Is continually exposed to populations where TB prevalence is high.

    Tuberculosis vaccine

    The first recombinant tuberculosis vaccine entered clinical trials in the United States in 2004 sponsored by the National Institute of Allergy and Infectious Diseases (NIAID). [1]

    History

    Tuberculosis has been present since antiquity - skeletal remains show prehistoric humans (4000 BC) had TB and tubercular decay has been found in the spines of Egyptian mummies from 3000-2400 BC. There were references to TB in India around 2000 BC and TB were in The Americas about 2000 BC

    Phthisis is a Greek term for consumption. Around 460 BC, Hippocrates identified phthisis as the most widespread disease of the times which was almost always fatal.

    Due to the variety of its symptoms, TB was not identified as a unified disease until the 1820s and was not named tuberculosis until 1839 by J.L. Schoenlein. Some forms of the disease were probably known to the ancient Greeks, if not before, as the origins of the disease are in the first domestication of cattle (which also gave humanity viral poxes).

    First TB sanatorium opened in 1859 in Poland; later, in 1885 in the United States.

    The bacillus-causing tuberculosis, Mycobacterium tuberculosis, was described on March 24, 1882 by Robert Koch. He received the Nobel Prize in physiology or medicine for this discovery in 1905. Koch did not believe that bovine (cattle) and human tuberculosis were similar, which held back the recognition of infected milk as a source of infection. Later, this source was eliminated by pasteurization. Koch announced a glycerine extract of the tubercle bacilli as a "remedy" for tuberculosis in 1890, calling it tuberculin. It was not effective, but was later adapted by von Pirquet for a test for pre-symptomatic tuberculosis.

    The first genuine success in immunizing against tuberculosis developed from attenuated bovine strain tuberculosis by Albert Calmette and Camille Guerin in 1906 was BCG (Bacillus of Calmette and Guerin). It was first used on humans on July 18, 1921 in France, although national arrogance prevented its widespread use in either the USA, Great Britain, or Germany until after World War II.

    Tuberculosis caused the most widespread public concern in the 19th and early 20th centuries as the endemic disease of the urban poor. In 1815 England one in four deaths were of consumption; by 1918 one in six deaths in France were still caused by TB. After the establishment in the 1880s that the disease was contagious, TB was made a notifiable disease in Britain; there were campaigns to stop spitting in public places, and the infected poor were "encouraged" to enter sanatoria that rather resembled prisons. Whatever the purported benefits of the fresh air and labour in the sanatoria, 75% of those who entered were dead within five years (1908).

    In the United States, concern about the spread of tuberculosis played a role in the movement to prohibit public spitting except into spittoons.

    In Europe, deaths from TB fell from 500 out of 100,000 in 1850 to 50 out of 100,000 by 1950. Improvements in public health were reducing tuberculosis even before the arrival of antibiotics, although the disease's significance was still such that when the Medical Research Council was formed in Britain in 1913 its first project was tuberculosis.

    It was not until 1946 with the development of the antibiotic streptomycin that treatment rather than prevention became a possibility. Prior to then only surgical intervention was possible as supposed treatment (other than sanatoria), including the pneumothorax technique: collapsing an infected lung to "rest" it and allow lesions to heal, which was an accomplished technique but was of little benefit and was discontinued after 1946.

    Hopes that the disease could be completely eliminated have been dashed since the rise of drug-resistant strains in the 1980s. For example, TB cases in Britain, numbering around 50,000 in 1955, had fallen to around 5,500 in 1987, but in 2001 there were over 7,000 confirmed cases. Due to the elimination of public health facilities in New York in the 1970s, there was a resurgence in the 1980s. The number of those failing to complete their course of drugs was very high. NY had to cope with more than 20,000 "unnecessary" TB-patients with many multi-drug resistant strains (i.e., resistant to, at least, both Rifampin and Isoniazid). The resurgence of tuberculosis resulted in the declaration of a global health emergency by the World Health Organization in 1993.

    In 2003, by disabling a set of genes, researchers accidentally created a more lethal and rapidly reproducing strain of tuberculosis bacteria.

    Christmas Seals was started in 1904 in Denmark as a way to raise money for tuberculosis programs. It came to the United States and Canada in 1907-08 to help the National Tuberculosis Association, later called the American Lung Association.

    Tuberculosis in art and literature

    It has been speculated that the real-life ubiquity of illness and death due to tuberculosis affected the portrayal of these issues in European art and literature.

    The Life and Death of Mr. Badman (1680) by John Bunyan - "Yet the captain of all these men of death that came against him to take him away, was the consumption, for it was that that brought him down to the grave."

    The pale, "haunted" appearance of tuberculosis sufferers has been seen as an influence on the works of Edgar Allan Poe and in vampire tales. In recent years, this aesthetic has been revived by the "Goth" subculture.

    The heroine, Mimi, of Puccini's opera La Bohème suffers from tuberculosis (a theme carried over in the modern film adaptation Moulin Rouge). Violetta, heroine of Verdi's La Traviata also dies of the disease.

    In Sylvia Plath's novel The Bell Jar, the protagonist Esther's boyfriend Buddy Willard suffers from tuberculosis, much to her liking.

    In Nicholas Nickleby, by Charles Dickens, Nickleby's faithful companion Smike is beset by tuberculosis.

    Extensively, in The Magic Mountain, by Thomas Mann, where a three week visit to a sanitarium turns into a seven year sabbatical.

    Tuberculosis patients were frequent characters in 19th century Russian literature, and even inspired a character type; the consumptive nihilist, examples of which include Bazarov from Ivan Turgenev's Fathers and Sons, and Kirillov from Fyodor Dostoevsky's Demons (aka The Possessed).

    The hospitalized mother in the anime movie My Neighbor Totoro is thought to be suffering from tuberculosis (her ailment is not specifically named in the film, but tuberculosis is cited in the film's novelization). This is an autobiographical reference to the fact that writer/director Hayao Miyazaki's own mother spent several years of his childhood hospitalized with TB.

    See also

    References

    External links

    Organizations

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