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American Heritage Dictionary:
tu·ber·cu·lo·sis |
[Latin tūberculum, tubercle; see tubercle + -OSIS.]
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Britannica Concise Encyclopedia:
tuberculosis |
For more information on tuberculosis, visit Britannica.com.
McGraw-Hill Science & Technology Encyclopedia:
Tuberculosis |
An infectious disease caused by the bacillus Mycobacterium tuberculosis. It is primarily an infection of the lungs, but any organ system is susceptible, so its manifestations may be varied. Effective therapy and methods of control and prevention of tuberculosis have been developed, but the disease remains a major cause of mortality and morbidity throughout the world. The treatment of tuberculosis has been complicated by the emergence of drug-resistant organisms, including multiple-drug-resistant tuberculosis, especially in those with HIV infection. See also Acquired immune deficiency syndrome (AIDS).
Mycobacterium tuberculosis is transmitted by airborne droplet nuclei produced when an individual with active disease coughs, speaks, or sneezes. When inhaled, the droplet nuclei reach the alveoli of the lung. In susceptible individuals the organisms may then multiply and spread through lymphatics to the lymph nodes, and through the bloodstream to other sites such as the lung apices, bone marrow, kidneys, and meninges.
The development of acquired immunity in 2 to 10 weeks results in a halt to bacterial multiplication. Lesions heal and the individual remains asymptomatic. Such an individual is said to have tuberculous infection without disease, and will show a positive tuberculin test. The risk of developing active disease with clinical symptoms and positive cultures for the tubercle bacillus diminishes with time and may never occur, but is a lifelong risk. Only 5% of individuals with tuberculous infection progress to active disease. Progression occurs mainly in the first 2 years after infection; household contacts and the newly infected are thus at risk.
Many of the symptoms of tuberculosis, whether pulmonary disease or extrapulmonary disease, are nonspecific. Fatigue or tiredness, weight loss, fever, and loss of appetite may be present for months. A fever of unknown origin may be the sole indication of tuberculosis, or an individual may have an acute influenzalike illness. Erythema nodosum, a skin lesion, is occasionally associated with the disease.
The lung is the most common location for a focus of infection to flare into active disease with the acceleration of the growth of organisms. There may be complaints of cough, which can produce sputum containing mucus, pus- and, rarely, blood. Listening to the lungs may disclose rales or crackles and signs of pleural effusion (the escape of fluid into the lungs) or consolidation if present. In many, especially those with small infiltration, the physical examination of the chest reveals no abnormalities.
Miliary tuberculosis is a variant that results from the blood-borne dissemination of a great number of organisms resulting in the simultaneous seeding of many organ systems. The meninges, liver, bone marrow, spleen, and genitourinary system are usually involved. The term miliary refers to the lung lesions being the size of millet seeds (about 0.08 in. or 2 mm). These lung lesions are present bilaterally. Symptoms are variable.
Extrapulmonary tuberculosis is much less common than pulmonary disease. However, in individuals with AIDS, extrapulmonary tuberculosis predominates, particularly with lymph node involvement. Fluid in the lungs and lung lesions are other common manifestations of tuberculosis in AIDS. The lung is the portal of entry, and an extrapulmonary focus, seeded at the time of infection, breaks down with disease occurring.
Development of renal tuberculosis can result in symptoms of burning on urination, and blood and white cells in the urine; or the individual may be asymptomatic. The symptoms of tuberculous meningitis are nonspecific, with acute or chronic fever, headache, irritability, and malaise.
A tuberculous pleural effusion can occur without obvious lung involvement. Fever and chest pain upon breathing are common symptoms.
Bone and joint involvement results in pain and fever at the joint site. The most common complaint is a chronic arthritis usually localized to one joint. Osteomyelitis is also usually present.
Pericardial inflammation with fluid accumulation or constriction of the heart chambers secondary to pericardial scarring are two other forms of extrapulmonary disease.
The principal methods of diagnosis for pulmonary tuberculosis are the tuberculin skin test (an intracutaneous injection of purified protein derivative tuberculin is performed, and the injection site examined for reactivity), sputum smear and culture, and the chest x-ray. Culture and biopsy are important in making the diagnosis in extrapulmonary disease.
A combination of two or more drugs is used in the initial therapy of tuberculous disease. Drug combinations are used to lessen the chance of drug-resistant organisms surviving. The preferred treatment regimen for both pulmonary and extrapulmonary tuberculosis is a 6-month regimen of the antibiotics isoniazid, rifampin, and pyrazinamide given for 2 months, followed by isoniazid and rifampin for 4 months. Because of the problem of drug-resistant cases, ethambutol can be included in the initial regimen until the results of drug susceptibility studies are known. Once treatment is started, improvement occurs in almost all individuals. Any treatment failure or individual relapse is usually due to drug-resistant organisms. See also Drug resistance.
The community control of tuberculosis depends on the reporting of all new suspected cases so case contacts can be evaluated and treated appropriately as indicated. Individual compliance with medication is essential. Furthermore, measures to enhance compliance, such as directly observed therapy, may be necessary. See also Mycobacterial diseases.
Oxford Companion to the Body:
tuberculosis |
Tuberculosis is caused by the microorganism Mycobacterium tuberculosis, or tubercle bacillus. It was in 1882 that Robert Koch, among his many historic contributions to bacteriology, identified this as the cause of the disease, thus firmly establishing for the first time its infective nature. It has been estimated that one-third of the world's population has been infected by M. tuberculosis but only a minority, probably about 10%, go on to develop disease. Disease manifests in any number of ways, almost all of them chronic, involving practically any part of the body. The most common site involved is the lungs, where cavities are produced. When this occurs patients have a cough with sputum (which sometimes contains blood), weight loss, and fever. Those with this type of disease are the most infectious, because of the presence of the bacillus in the sputum. Animals also carry the disease; although Koch had denied the possibility, it was later realized that the bovine strain of the organism, Mycobacterium bovis, could cause human infection from cow's milk.
Historically, tuberculosis has long ranked among the most feared of diseases. Such dread is reflected in some of its alternative names, including John Bunyan's ‘Captain of all these Men of Death’, and Charles Dickens' ‘dread disease’ which capture something of the prevalence of the disease in their times. Other names conjure up images of the disease process: the term ‘consumption’ describes what happened to an individual — a progressive emaciation and wasting away. Still other terms, such ‘the King's Evil’ describe the lottery of survival (cure arising from the king's touch in medieval England). Yet tuberculosis is not only a disease of the past. Keats' ‘death warrant’ continues to haunt us. Historically tuberculosis conjures up romantic images of pale, wraith-like artists suffering lingering deaths. Literature, art, and music have all recorded and been transformed by the disease. Those who have succumbed to the disease form a veritable who's who of the artistic and political worlds and notions persist that those with artistic leanings are at greater risk from tuberculosis. As Susan Sontag noted in Illness as Metaphor, ‘tuberculosis was thought to come from too much passion, afflicting the reckless and sensual.’ Gradually, however, perceptions changed. In the US, for example, Katherine Ott noted in Fevered Lives that this ‘most flattering of all diseases’ of the 1870s was transformed, as awareness of the social associations grew in the 1880s, into a disease which was seen as the consequence of either acquired or inherited degeneracy and later came to mirror ethnic and racial fears and prejudices. Yet by the turn of the century the enthusiasm for pointing the finger at individual weaknesses was tempered by an increasing awareness that society's strictures were in part responsible. In truth, in past centuries tuberculosis was a frequent killer of people from all walks of life, not only the famous and infamous, the artistic and notorious. Those living in poverty and squalor were always most susceptible.
The sanatorium movement, which promoted wholesome rest and genteel exercise in pleasant surroundings, took off in the second half of the nineteenth century. In Britain, which borrowed the idea from Germany, the first sanatoria opened in the 1890s. Although many sanatoria in Europe catered for a select, affluent, cosmopolitan clientele (an image which persists in the popular imagination conjured up by establishments such as those at Davos in Switzerland), sanatorium treatment also, by the 1920s, became available for those unable to pay, and the average duration of stay shortened. However a decline in the sanatorium movement started with the onset of World War I and was hastened by the Depression which followed. Although there were still thousands of tuberculosis sufferers receiving care in sanatoria by the mid 1940s, the availability of effective drug treatment meant that they soon became obsolete. Removal of infectious sufferers from the community had contributed to a decrease in incidence of the disease, but for the patients in sanatoria or specialized hospitals there was no specific cure. Recovery was sometimes assisted by causing collapse of an infected lung by the introduction of air into the chest (artificial pneumothorax) or by an operation that ‘caved-in’ the overlying ribs (thoracoplasty).
The advent of drug treatment followed the discovery, by Selman Waksman in the US in 1944, that streptomycin was effective, and other drugs shortly followed. When chemotherapy from then on resulted in cure for most tuberculosis sufferers, contemporary commentators told stories largely of hope, of medicine's conquest of nature, and reflected less on societal hindrances to medicine's application. An optimistic faith in the benefits of science shone through such that it seemed merely a matter of time before this ancient scourge would be eradicated. At the time this optimism seemed well-founded: mortality rates in England and Wales, which had been falling by about 1% annually since the 1860s, declined dramatically from the mid 1940s. Death rates for respiratory tuberculosis in England and Wales were about 125/100 000 at the turn of the century, and by the 1960s had fallen to below 10/100 000. Preceding the advent of chemotherapy there had been improvements in social conditions and better identification of those with active disease, along with advances in bacteriology and in X-ray diagnosis. From the 1920s there were attempts to control bovine infection, first by certifying tuberculin tested (TT) herds, and later by heat treatment to kill bacteria in milk. Although this pasteurization had been considered as early as 1913, Britain lagged behind much of Europe and the US by more than a quarter of a century in putting it into consistent effect. A further preventative measure was the introduction in the 1950s of the BCG (Bacille Calmette Guérin) vaccination programme.
Despite the remarkable success in controlling tuberculosis in the West, the overriding optimism which followed the development of effective antituberculosis drugs in the 1940s and 1950s was somewhat premature. The disease continues to target those most marginalized and vulnerable. Each year more than 8 million people acquire tuberculosis (most of them in the developing world), and about 3 million die, including about 100 000 children, annually. In England and Wales there was concern as to why this should be, why Keats' death warrant should still be received by so many, given that we have had at our disposal for over fifty years drugs which are effective in curing the disease? The answer was known half a century ago.
‘Tuberculosis is a social disease, and presents problems that transcend the conventional medical approach. On the one hand, its understanding demands that the impact of social and economic factors on the individual be considered as much as the mechanisms by which tubercle bacilli cause damage to the human body. On the other hand, the disease modifies in a peculiar manner the emotional and intellectual climate of the societies that it attacks.’ Rene Dubos who, with his wife Jean, wrote these words in 1952, was one of the giants of twentieth-century medicine. As well as being a major figure in the development of antibacterial drugs in the US in the 1920s and 1930s, which led to the later successful antituberculous drugs, he was able, unlike so many, to see the place of tuberculosis in society and to recognize the limits of modern medicine. His words resonate through the years and perhaps are more pertinent now than ever. In 1993 the World Health Organization officially called the global threat of tuberculosis an ‘emergency’. New drug-resistant strains of the organism are spreading and modern medical approaches are failing to cure patients. In England and Wales there was a 20% increase in incidence of the disease between 1987 and 1990, weighted towards the underprivileged. Overcrowding, poverty, social alienation, increased incarceration rates in prisons, homelessness, and AIDS (the ‘deadly alliance’) are combining to overwhelm uncoordinated and under-resourced public health responses.
Perhaps nowhere have the consequences of contemporary public health failures been more obvious than in New York City. In the late 1980s and early 1990s an epidemic of this ancient disease killed hundreds of people, forcing politicians to rethink their approaches to those living on the margins of society, and provoking a response which has cost millions of dollars. As Rene Dubos knew all along, tuberculosis is as much a social and political disease as it is a medical condition.
— Richard Coker
Bibliography
See also infectious diseases; immunization.
Roget's Thesaurus:
tuberculosis |
noun
Oxford A-Z of Medicinal Drugs:
tuberculosis |
| tryptophan, trospium chloride, tropicamide | |
| turpentine oil, tyrosine kinase inhibitors, tyrothricin |
Gale Encyclopedia of Children's Health:
Tuberculosis |
Definition
Tuberculosis is a chronic, infectious disease that primarily attacks the lungs.
Description
Tuberculosis (TB) is caused by a bacteria that primarily attacks the lungs. An individual may be "TB infected," meaning the bacteria are in the body but are in an inactive state, walled off behind scab-like structures that are the body's defense mechanism, or have "TB disease," when the bacteria actively spread throughout the body and can cause damage to the lungs or other organs. The severity of the attack depends on whether the bacteria spread from the lungs to other parts of the body. TB infection in the blood, the meninges (membranes around the brain and spinal cord), or the kidneys are the most serious. Children between the ages of six and 24 months are the most susceptible to meningitis; it is the chief cause of tuberculin death among children.
Transmission
The bacteria that causes TB, Mycobacterium tuberculosis, is transmitted by droplets when an infected person coughs or sneezes. It is not spread through kissing or other physical contact. Children nearly always contract the disease from an infected adult.
Demographics
In 2003, the Centers for Disease Control and Prevention (CDC) reported 14,874 cases of tuberculosis in the United States, or 5.1 cases per 100,000 population. The actual number of TB infections, however, is estimated to be much higher, as high as ten million. In 2002, there were 802 tuberculosis-related deaths. The District of Columbia had the highest rates of TB, with 14 cases per 100,000 people in 2003; Montana and Wyoming had the lowest rate, with 0.8 cases per 100,000 population. Children less than 15 years of age represented 6 percent of reported TB cases, and 15–24-year-olds represented 11 percent of all cases. Worldwide, TB cases are the rise, with nearly 8.8 million new cases a year being estimated by the World Health Organization (WHO).
Causes and Symptoms
Mycobacterium tuberculosis is a microscopic, rod-shaped bacterium. The majority of individuals who are infected with TB do not go on to have active disease. Active TB can be triggered when a person's immune system is weakened, such as from human immunodeficiency virus (HIV), malnutrition, or alcohol abuse.
Early symptoms of TB include unusual fatigue, fever, loss of weight, headache, coughing, and irritability. An infected child may have night sweats and cough up blood. In advanced stages, the patient will suffer persistent coughing, breathlessness, and fever. Many times TB is not diagnosed and becomes dormant; this is known as initial tuberculosis. In severe cases among young children between the ages of two and four, initial TB can be fatal. The disease can reoccur, or reactivate, during adolescence when resistance is low, and may disappear on its own or develop into serious lung disease.
When to Call the Doctor
Parents should contact their child's doctor if the child has been in contact with someone who has been diagnosed with or is suspected to have tuberculosis, or if the child exhibits the symptoms of the disease, particularly persistent fever, night sweats, and cough.
Diagnosis
Tuberculosis is nearly always diagnosed by tuberculin skin tests, although one can also be diagnosed by chest x rays and analysis of sputum (matter from the respiratory tract) smears and cultures. The most common tuberculin skin test is the Mantoux test, which consists of injecting a small amount of protein from the TB bacillus into the forearm. A reddening and swelling of the area after 24–72 hours signals the presence of TB. A negative result, however, may not necessarily exclude a diagnosis of TB.
Treatment
The disease is treated with a regimen of strong antibiotics such as Rifampin and Isoniazid for six months to two years. Because some strains of the disease are unusually drug-resistant, cultures are grown from the patient's bacteria and tested with a variety of drugs to determine the most effective treatment. In cases of strong drug-resistant strains, the child may undergo surgery to remove the infected areas.
Infants with TB are usually hospitalized but children and teenagers can generally lead active lives within two weeks of beginning medication. It is imperative that the mediation prescribed be taken faithfully.
Prognosis
With treatment, TB infection that is not drug resistant can nearly always be cured as long as patients are consistent with their medications and considerable lung damage as not already occurred. Drug-resistant TB has a lower cure rate. Without treatment, the disease will continue to progress; approximately one-half of untreated TB patients will die of the disease.
Prevention
Stopping the spread of tuberculosis is the most effective way of preventing its incidence among children. All adults who work with children should be screened regularly. In many communities, children are tested when they reach their first birthday and then at one-to-three year intervals throughout the school years. The medical profession is divided on the issue of screening; some physicians believe that the screening should be focused in areas of common occurrence or within high-risk populations such as foreign-born children. The practice of relying on parents to report results of the skin testing has also come under criticism from some members of the medical community.
While a vaccine for TB does exist (Bacille Calmette-Guerin or BCG vaccine), it is not widely available in the United States and has had conflicting reports about its efficacy. Being inoculated with BCG vaccine does not always prevent infection with the disease. The vaccine is only recommended for children in the United States if they live with someone who has active TB that cannot be treated or is drug-resistant.
Nutritional Concerns
Poor nutrition is closely related active tuberculosis; children with adequate nutrition are more resistant to the disease than those who suffer from malnutrition.
Parental Concerns
If a child has been infected with TB and is prescribed drug therapy to treat the disease, it is imperative that parents closely monitor their child to ensure that the medication is taken as prescribed; if the medication is not taken frequently enough or until it is no longer needed, drug-resistant TB can arise.
Resources
Books
Landau, Elaine. Tuberculosis. New York: F. Watts, 1995.
Periodicals
"TB on the Rise." Patient Care 38, no. 6 (June 2004): 9-10.
Young, Douglas B. and Brian D. Robertson. "TB Vaccines: Global Solutions for Global Problems." Science 284, no. 5419 (May 28, 1999): 1479.
Organizations
American Lung Association. 61 Broadway, 6th Floor, New York, NY 10006. (800) 548-8252. Web site: www.lungusa.com.
Centers for Disease Control and Prevention. 1600 Clifton Rd., Atlanta, GA 30333. (404) 639-3311. Web site: www.cdc.gov.
Web Sites
Division of Tuberculosis Elimination. "Reported Tuberculosis in the United States, 2003." Centers for Disease Control and Prevention. [cited September 12, 2004]. Available online at:
Sharma, Sat. "Tuberculosis." eMedicine. January 14, 2003 [cited September 12, 2004]. Available online at: www.emedicine.com/aaem/topic464.htm.
[Article by: Mary McNulty Stephanie Dionne Sherk]
Gale Encyclopedia of Public Health:
Tuberculosis |
Tuberculosis (TB), an infectious disease, has been present throughout ancient and modern history. TB rates in the United States are on the decline after a resurgence from 1985 to 1992. However, TB continues to be a major killer in much of the world. The implications of this epidemic are global, as travel and migration are now part of everyday life.
Although the cause, diagnosis, and treatment and prevention of TB are known, paradoxically, the disease continues to increase as a public health challenge. Caused by a bacterium called Mycobacterium tuberculosis, TB spreads via an airborne route from an infectious person coughing, sneezing, laughing, or singing. The bacteria infect mainly other individuals who have frequent and prolonged contact with a contagious TB case.
History
TB's existence dates back many centuries. There are references to TB in third-century B.C.E. Chinese and second-century B.C.E. Indian texts; Plato and Hippocrates wrote about it around 400 B.C.E. TB was commonly known as consumption in Europe, a cause of death for hundreds of thousands in the late eighteenth and nineteenth centuries. This is when TB in close groups was first observed and assumed to have a genetic cause, since it was commonly seen in families.
In 1882 Robert Koch's discovery of Mycobacterium tuberculosis led to the recognition of TB as an infectious disease. This discovery also led to interventions for interrupting transmission from person-to-person.
Beginning in the late 1880s, TB patients were treated in sanitoria with various modalities, including exposure to fresh air, exercise, and nourishment. About 50 percent of patients recovered or had long-term remission. However, as is known today, their "cure" was not due to the treatments administered but perhaps to self-healing mechanisms.
In the early twentieth century, public health interventions became key in controlling the spread of TB in the cities, where TB was most prevalent. For example, Herman M. Biggs, General Medical Officer of New York City, actively catalogued lists of TB patients and enforced isolation and environmental mechanisms to control TB, including the opening of a TB hospital to quarantine patients. Between 1914 and 1923, the Metropolitan Life Insurance Company conducted the "Framingham Tuberculosis Project" using community nurses to visit the homes of its clients to do assessments, teach health practices, and collect data for research and policy-making purposes. The project was in response to a high rate of TB-related mortality among Metropolitan customers. As a result, mortality rates for TB in the Metropolitan pool declined by 68 percent.
Beginning in 1921, the Bacille Calmette Guerin (BCG) vaccine was used to prevent TB. Still used in many parts of the world but not in the United States, the vaccine is not effective, except perhaps in infants. The discovery of streptomycin in 1943 brought drug treatment for TB. Between 1943 and 1952, two more TB drugs, para-amino-salicylic acid (PAS) and isoniazid (INH), were discovered. Sanitoria began to close in the early 1970s, as TB could be now be treated on an outpatient basis, as evidenced by success in the decrease in TB rates with combined drug treatment and infection-control mechanisms.
Resurgence
By 1985, there were 22,201 cases of TB in the United States, the lowest number recorded since national case reporting began in 1953. However, rates then began to increase, until in 1992 cases peaked at 26,673. The human immunodeficiency virus (HIV) epidemic was a major contributor, as its victims are at higher risk for developing active disease once infected with TB bacteria. Migration from countries with high rates of TB added to the number. Also, improper or inadequate drug treatment for TB has led to drug-resistant strains. Finally, medical education stressed TB to a lesser degree in academic curricula, and funding and interest in TB-control programs had dwindled with decreased cases. Most authorities feel that the latter reason was the most important.
Response to the American TB resurgence resulted in increased funding for TB control programs. This gave greater access to TB treatment through health departments. The health departments were responsible not only for treating cases, but for surveillance, outreach, case management, and treatment for those who had been exposed to infectious TB cases. Directly observed therapy short course (DOTS), the observation of the ingestion of medication, has now become the basis for the worldwide standard of TB care. DOTS includes five elements: government commitment to sustained TB-control activities; case detection and self-reporting to health services; standardized treatment regimen of six to eight months for at least all confirmed infectious cases, with directly observed treatment (DOT) for at least the initial two months; a regular, uninterrupted supply of all essential anti-TB drugs; and a standardized recording and reporting system that allows assessment of treatment results for each patient and of the TB control program overall. DOTS is presently available to 25 percent of the world's TB patients, but its acceptance is slowly increasing. There was also an increase in TB educational interventions via the public health sector and medical schools. New drug trials did not create new drugs but created variations on existing drugs and regimens. TB rates began to decrease again in 1994, and as of 1999, they were at an all-time low of 17,528 cases in the United States. Globally, there are still eight million new cases of TB annually with three million deaths. Clearly, even with the exemplary level of achievement domestically, TB cannot be controlled anywhere unless it is controlled everywhere.
The Future
Although one of the Healthy People 2010 goals calls for TB elimination from this country, the United States is still far from that goal. Many interventions need to be continued despite falling rates. For other communicable diseases, effective vaccine development and the advent of new drug therapies has been key to disease control approaching elimination. The best course for TB elimination is to develop a vaccine and new drugs while continuing surveillance, treating TB patients who may infect others, treating those who have been infected but are not yet active cases, increasing TB awareness among health professionals, and performing targeted testing for TB infection among high-risk populations. This combination of medical and public health practice can make TB elimination a reality.
(SEE ALSO: Communicable Disease Control; Drug Resistance; Immunizations; Isolation)
Bibliography
Centers for Disease Control and Prevention (1995). Self-Study Modules on Tuberculosis. Atlanta, GA: Author.
—— (2000). Core Curriculum on Tuberculosis: What the Clinician Should Know, 4th edition. Atlanta, GA: Author.
Daniel, T. M. (1997). Captain of Death: The Story of Tuberculosis. Rochester, NY: University of Rochester Press.
Dublin, L. I. (1952). A Forty-Year Campaign against Tuberculosis: The Contribution of the Metropolitan Life Insurance Company. New York: Metropolitan Life Insurance Company.
Reichman, L. B. and Tanne J. H. (2001). Time Bomb: The Global Epidemic of Multidrug Resistant Tuberculosis. New York: McGraw Hill.
— RAJITA R. BHAVARAJU; LEE B. REICHMAN
Gale Encyclopedia of US History:
Tuberculosis |
Tuberculosis was the leading cause of death in the United States during the nineteenth century, responsible at times for as many as one of every four deaths. Although the death rate from tuberculosis steadily declined beginning in the mid-nineteenth century, it persisted as a major public health problem well into the twentieth century, when programs of public health education, disease surveillance and diagnosis, and the availability of antibiotics and vaccination helped to curb its incidence. After World War II, the death rate was only a small fraction of what it was a century earlier, but by the 1990s, the emergence of tuberculosis strains resistant to antibiotics and the connections between tuberculosis and AIDS again made it a significant health concern.
Before the late nineteenth century, various names—including consumption and phthisis—were used to describe the dry, persistent cough, throat irritations, chest and shoulder pains, and difficult breathing accompanied by emaciation that characterized pulmonary tuberculosis. The incidence of tuberculosis grew dramatically in Europe beginning in the eighteenth century, and although its incidence in the United States was less severe, it had grown into the leading cause of death in the United States by the mid-nineteenth century. Other than being slightly more prevalent in women than men, the disease respected no boundaries, afflicting Americans of all ages, races, ethnicities, and social and economic stations.
Tuberculosis in Nineteenth-Century Life
While sudden and dramatic epidemics of cholera, diphtheria, smallpox, and yellow fever commanded public attention, tuberculosis quietly became a regular feature of nineteenth-century American life. Healers diagnosed tuberculosis on the basis of its physical symptoms, but they were at a loss to offer a definitive cause or cure for the disease. For much of the nineteenth century, it was thought that tuberculosis was hereditary, and therefore, that it was noncontagious and could not be transmitted from person to person. It was presumed that there was some familial disposition that made a person susceptible to the disease and that the interaction of the inherited constitution with environmental or behavioral "irritations," such as rich diets, sedentary occupations, and cold, wet climates, brought on the disease. The remedies emphasized changing the irritants, whether to a mild or bland diet, to an active lifestyle with exercise, or to a residence that was mild and dry. Between 1840 and 1890, thousands of Americans with tuberculosis, particularly from New England, became "health seekers," moving to where they believed the wholesome, restorative climates would give them relief. These "lungers," as tuberculosis patients were colloquially called, moved first to Florida, and later to the West and Southwest, settling in the deserts and mountains of Arizona, California, Colorado, and New Mexico. One in four migrants to California and one in three migrants to Arizona during the second half of the nineteenth century went looking to improve their health.
During the 1830s, tuberculosis was responsible for one in every four deaths, but by the 1880s, the mortality rate had declined to one in every eight deaths. In major American cities, the death rate from tuberculosis at the end of the nineteenth century (200 deaths per 100,000 population) was essentially half of what it was a century earlier. Improvements in diets and in living conditions, along with natural selection and genetic resistance in the population, contributed to the declining rates. Even as the mortality rates from tuberculosis declined in the general population, it persisted as a significant health problem among America's growing immigrant population, most of whom lived in the crowded, dank, and dirty tenements of America's urban centers—living conditions that were ripe for the rapid spread of the disease. The incidence of tuberculosis became increasingly associated with immigrants and the impoverished and the overcrowded living conditions they experienced.
Tuberculosis in the Age of Bacteriology
In March 1882, the German bacteriologist Robert Koch announced the discovery of Mycobacterium tuberculosis, the bacillus or bacterium that causes tuberculosis. But medical explanations attributing the cause of tuberculosis to heredity, climate, diet, lifestyle, poor ventilation, and other factors endured through the century and decades would pass before physicians were fully convinced that tuberculosis was contagious and could be transmitted between persons. The medical landmark of Koch's discovery accompanied the growing number of tuberculosis sanatoria being built in Europe and the United States after the 1850s and 1880s, respectively. The sanatorium movement emphasized a therapy regimen based on fresh air, proper diet, and rest, but they also served to remove and to isolate patients with tuberculosis from areas where they might infect others. Among the sanatoria were two founded by America's most prominent physicians of tuberculosis: Edward Livingston Trudeau established a sanatorium at Saranac Lake in the Adirondack Mountains of northeastern New York, and Lawrence Flick established a sanatorium at White Haven, in the Pocono Mountains of eastern Pennsylvania. Trudeau and Flick themselves suffered from tuberculosis, and learned of the benefits of an outdoor life in seeking a cure for their own afflictions. Trudeau's Saranac Lake sanatorium, founded in 1884, became a model for other sanatoria. Flick, believing that tuberculosis was contagious, advocated for a scientific approach to its diagnosis and treatment, as well as the registration of patients and the education of the public about the disease. In 1892, Flick founded the Pennsylvania Society for the Prevention of Tuberculosis, the first state organization in the nation devoted to the control and the elimination of tuberculosis. As other state societies against tuberculosis developed, Flick joined Trudeau, Hermann Biggs, William Welch, William Osler, and others to found in 1904 the National Association for the Study and Prevention of Tuberculosis (NASPT), the forerunner to the American Lung Association, which unified efforts, led public health education campaigns, and raised funds for research.
By the turn of the twentieth century, as the presence of the tubercle bacillus rather than the physical symptoms became the basis for diagnosis, the new understanding of what caused tuberculosis and how it was spread brought important changes in public health and the medical care of patients. The goal of Progressive Era public health work against tuberculosis was to improve social conditions and to control the behaviors that fostered the disease. Health departments instituted education campaigns that used films, posters, and lectures to dissuade individuals from practices that spread germs, such as spitting and coughing. In addition to maintaining clean, well-ventilated homes, the use of nonporous building materials such as metals, linoleum, and porcelain was encouraged over wood and cloth, which could harbor disease-causing germs. Public health officials inspected and fumigated dwellings that posed health risks, required physicians to report cases of tuberculosis, and forcibly isolated individuals who did not seek treatment. New diagnostic tests such as the tuberculin skin test and radiological examinations were used in mass screenings for tuberculosis, and new surgical therapies involving the collapse or partial section of the lungs were introduced. Infected individuals were required to seek treatment through a sanatorium or through a dispensary that engaged in disease surveillance and patient education.
Tuberculosis After World War II
The result of the far-reaching and aggressive public health campaign was that the incidence of tuberculosis, which had been steadily declining since the 1870s (when the mortality rate exceeded 300 deaths per 100,000 population), fell to unprecedented low levels by the 1930s (when the mortality rate fell below 50 deaths per 100,000 population). Disease mortality fell even lower (to 10 deaths per 100,000 population in 1954) after the development of an antibiotic, streptomycin, by the microbiologist Selman Waksman in 1943. Although other countries in the 1950s instituted vaccination campaigns using the Bacillus-Calmette-Guérin (BCG) vaccine, it was not adopted for wide use in the United States as public health programs emphasized the identification of patients exposed to the bacillus rather than universal vaccination against the disease.
Between 1954 and 1985, the incidence of tuberculosis in the United States declined 75 percent, and by 1989, public health officials confidently predicted its eradication in the United States by 2010 and worldwide by 2025, believing it would no longer pose a public health threat. These expectations were dashed as a worldwide pandemic of tuberculosis began in 1987 and the World Health Organization declared that tuberculosis posed a global emergency in 1993. The displacement of populations through immigration and political conflicts; the emergence of drug-resistant strains; the high rates of incarceration, homelessness, and intravenous drug use; the prevalence of mass air travel; the collapse of medical services in eastern Europe; the persistence of widespread poverty; and the progress of the AIDS pandemic, in which tuberculosis emerged as an opportunistic infection, all contributed to a worldwide public health crisis. By 2002, the World Health Organization reported that tuberculosis was the leading infectious killer of youth and adults and a leading killer of women, and that a third of the world's population was infected with the tuberculosis bacillus. In response, nearly 150 countries, including the United States, agreed to adopt the Directly Observed Treatment Short-Course (DOTS) system in which countries would promote public health programs of case detection, standardized treatment regimens using multiple drugs, patient surveillance to monitor compliance, and the forcible detention of noncompliant patients. Once thought to be on the verge of eradication, in 2002 it was not known if and when the worldwide incidence of tuberculosis would return to levels experienced only a half century before.
Bibliography
Bates, Barbara. Bargaining for Life: A Social History of Tuberculosis, 1876–1938. Philadelphia: University of Pennsylvania Press, 1992.
Ellison, David L. Healing Tuberculosis in the Woods: Medicine and Science at the End of the Nineteenth Century. Westport, Conn.: Greenwood Press, 1994.
Feldberg, Georgina. Disease and Class: Tuberculosis and the Shaping of Modern North American Society. New Brunswick, N.J.: Rutgers University Press, 1995.
Lerner, Barron H. Contagion and Confinement: Controlling Tuberculosis Along the Skid Road. Baltimore: Johns Hopkins University Press, 1998.
Ott, Katherine. Fevered Lives: Tuberculosis in American Culture since 1870. Cambridge, Mass.: Harvard University Press, 1996.
Rothman, Sheila. Living in the Shadow of Death: Tuberculosis and the Social Experience of Illness in America. New York: Basic Books, 1994.
Ryan, Frank. The Forgotten Plague: How the Battle against Tuberculosis Was Won—And Lost. Boston: Little, Brown, 1993.
Teller, Michael. The Tuberculosis Movement: A Public Health Campaign in the Progressive Era. New York: Greenwood Press, 1988.
Columbia Encyclopedia:
tuberculosis |
There are three major types of tubercle bacilli that affect humans. The human type (Mycobacterium tuberculosis), first identified in 1882 by Robert Koch, is spread by people themselves. It is the most common one. The bovine type (M. bovis) is spread by infected cattle but is no longer a threat in areas where pasteurization of milk and the health of cattle are strictly supervised. The avian type (M. avis) is carried by infected birds but can occur in humans. The tubercle bacillus can live for a considerable period of time in air or dust. The most common means of acquiring the disease is by inhalation of respiratory droplets.
Course of the Disease
Tuberculosis of the lungs usually results in no or minimal symptoms in its early stages. In most persons the primary infection is contained by the body's immune system, and the lesion, called a tubercle, becomes calcified. In many the infection is permanently arrested. In others the disease may break out again and become active years later, usually when the body's immune defenses are low. Untreated, the infection can progress until large areas of the lung and other organs are destroyed. Symptoms of the disease include cough, sputum, bleeding from the lungs, fever, night sweats, loss of weight, and weakness.
Incidence
The incidence of tuberculosis of the lungs, the "white plague" that formerly affected millions of people, declined from the 1950s until 1984; sanatoriums were closed and routine screening was abandoned in the United States. Then, between 1984 and 1992, the incidence increased by 20%, chiefly because of immigration from countries where it is common and because of AIDS, which leaves people particularly vulnerable to the disease. Renewed efforts at control and advances in treatment have been rewarded with incidence declines each year, amounting to a total decline of 31% from 1992 to 1998.
Worldwide the outlook has been far less encouraging. In 1993 the World Health Organization (WHO) declared TB a global health emergency. Approximately one third of the world's population is infected, and an estimated 1.6 million die each year. The vast majority of new cases occur in sub-Saharan Africa. Spread of TB is especially rapid in areas with poor public health services and crowded living conditions. In homeless shelters and prisons, crowded conditions and inadequate treatment often go together. Areas where living conditions are disrupted by wars, famine, and natural disasters also are heavily affected.
Especially alarming has been the spread of drug-resistant strains of TB. By the late 1990s scientific experts and international health officials warned that drug-resistant strains were spreading faster than had been anticipated. Bacteria can survive and become drug resistant in patients whose treatment is not properly monitored and seen to completion. Multidrug resistant (MDR) TB strains are resistant to two or more of the commonly prescribed first-line drugs, while extensively drug resistant (XDR) strains are also resistant to three or classes of the more toxic second-line drugs. Some believe that unless major new treatment strategies are initiated in source countries, drug-resistant TB will eventually become epidemic even in areas with good control programs, such as Europe and America. In 2011, WHO estimated that there were more than 80,000 cases, many of them undiagnosed, of drug-resistant TB in Europe.
Diagnosis and Treatment
Diagnosis is made by a tuberculin skin test. It can be confirmed by X rays of the chest and sputum examination. Ideally, treatment begins after a skin test signals exposure but before active disease has developed. The treatment of choice for prevention and for active cases is the antimicrobial drug isoniazid (INH), available since 1956. In infected individuals it now is usually used in combination with other antituberculosis drugs such as rifampin, pyrazinamide, and ethambutol. Tuberculosis drugs have to be taken regularly, typically for 6 to 12 months. Many patients abandon their treatment when they feel better; similarly, preventive treatment is often abandoned because of the inconvenience. Such noncompliance is believed to be the main reason for the upsurge in drug-resistant strains of the TB bacilli, many of which are resistant to more than one drug. Drug-resistant TB is difficult to treat and has a much higher death rate; extensively drug resistant TB is especially worrisome because it can be essentially untreatable.
The combination drug rifater (rifampin, isoniazid, and pyrazinamide) has simplified drug administration. Directly observed treatment, where health-care workers watch patients take each dose of medicine, has proved effective in eliminating the problem of noncompliance in the United States, but monitoring has been less effective in many other parts of the world.
Prevention of Tuberculosis
Preventive measures include strict standards for ventilation, air filtration, and isolation methods in hospitals, medical and dental offices, nursing homes, and prisons. If someone is believed to have been in contact with another person who has TB, preventive antibiotic treatment may have to be given. Infected persons need to be identified as soon as possible so that they can be isolated from others and treated.
An antituberculosis vaccine, bacille Calmette-Guérin, or BCG vaccine, was developed in France in 1908. Although there is conflicting evidence as to its efficacy (it appears to be effective in 50% of those vaccinated), it is given to over 80% of the world's children, mostly in countries where TB is common; it is not generally given in the United States. Federal health officials in the United States have stated (1999) that a new vaccine is essential to TB prevention. It is hoped that the determination of the complete DNA (genome) sequence of Mycobacterium tuberculosis, achieved in 1998, will hasten the development of an effective vaccine.
Bibliography
See R. Dubos, The White Plague (1955); S. A. Waksman, The Conquest of Tuberculosis (1964).
Dictionary of Cultural Literacy: Health:
tuberculosis |
An infectious disease caused by bacteria that mainly attack the lungs. The disease is characterized by the formation of patches, called tubercles, that appear in the lungs and, in later stages, the bones, joints, and other parts of the body. Tuberculosis is treated with combinations of antibiotics and is no longer considered a major health problem in industrialized countries. It was formerly called consumption.
Saunders Veterinary Dictionary:
tuberculosis |
Applied generally to diseases caused by tuberculous group of bacteria in the genus Mycobacteria, which includes Mycobacteria tuberculosis, M. bovis and M. avium. See also fish tuberculosis, mycobacteriosis.
Mosby's Dental Dictionary:
tuberculosis |
An infectious disease caused by Mycobacterium tuberculosis and characterized by the formation of tubercles in the tissues.
Tuberculosis of tongue. (Regezi/Sciubba/Pogrel, 2000)
Random House Word Menu:
categories related to 'tuberculosis' |
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tuberculosis |
Bradford's Crossword Solver's Dictionary:
tuberculosis |
See crossword solutions for the clue Tuberculosis.
Wikipedia on Answers.com:
Tuberculosis |
| Tuberculosis | |
|---|---|
| Classification and external resources | |
 Chest X-ray of a person with advanced tuberculosis |
|
| ICD-10 | A15–A19 |
| ICD-9 | 010–018 |
| OMIM | 607948 |
| DiseasesDB | 8515 |
| MedlinePlus | 000077 000624 |
| eMedicine | med/2324 emerg/618 radio/411 |
| MeSH | D014376 |
Tuberculosis, MTB, or TB (short for tubercle bacillus) is a common, and in many cases lethal, infectious disease caused by various strains of mycobacteria, usually Mycobacterium tuberculosis.[1] Tuberculosis usually attacks the lungs but can also affect other parts of the body. It is spread through the air when people who have an active MTB infection cough, sneeze, or otherwise transmit their saliva through the air.[2] Most infections in humans result in an asymptomatic, latent infection, and about one in ten latent infections eventually progress to active disease, which, if left untreated, kills more than 50% of those infected.
The classic symptoms are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss (the last giving rise to the formerly prevalent colloquial term "consumption"). Infection of other organs causes a wide range of symptoms. Diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids. Treatment is difficult and requires long courses of multiple antibiotics. Social contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensively) multi-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin vaccine.
One third of the world's population is thought to have been infected with M. tuberculosis,[3][4] and new infections occur at a rate of about one per second.[3] In 2007 there were an estimated 13.7 million chronic active cases,[5] and in 2010 8.8 million new cases, and 1.45 million deaths, mostly in developing countries.[6] The absolute number of tuberculosis cases has been decreasing since 2006 and new cases since 2002.[6] In addition, more people in the developing world contract tuberculosis because their immune systems are more likely to be compromised due to higher rates of AIDS.[7] The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries test positive in tuberculin tests, while only 5–10% of the U.S. population test positive.[1]
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Only about 5-10% of those infected with tuberculosis, without HIV, develop active disease.[9] In contrast 30% of those co-infected with HIV develop active disease.[9] Extrapulmonary TB may co-exist with pulmonary TB.[10]
If tuberculosis does become active, it most commonly involves infection in the lungs (pulmonary TB).[7] Symptoms include chest pain and a productive, prolonged cough. About a quarter of people however may not have any symptoms.[7] Occasionally people may cough up blood in small amounts and in very rare cases the infection may erode into the pulmonary artery resulting in massive bleeding known as Rasmussen's aneurysm.[10] Spitting up stones known as lithoptysis has been described due to bronchial lymph nodes communicated with the airways.[10] Tuberculosis may become chronic with scarring usually in the upper lobes of the lungs.[10] It is believed that the upper lungs are more frequently affected due to their poor lymph supply rather than more air flow.[10]
In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted extrapulmonary tuberculosis.[11] This occurs more commonly in immunosuppressed persons and young children. Extrapulmonary infection sites include the pleura in tuberculous pleurisy, the central nervous system in meningitis, the lymphatic system in scrofula of the neck, the genitourinary system in urogenital tuberculosis, and the bones and joints in Pott's disease of the spine. When spread to the bones it is also known as "osseous tuberculosis",[12] a form of osteomyelitis (as a complication of tuberculosis[1]). A potentially more serious form is disseminated TB, more commonly known as miliary tuberculosis.[10]
Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, and fatigue.[10] Finger clubbing may also occur.[9]
The main cause of TB is, Mycobacterium tuberculosis, a small aerobic non-motile bacillus or less commonly the closely related Mycobacterium bovis.[10] The high lipid content of this pathogen accounts for many of its unique clinical characteristics.[13] It divides every 16 to 20 hours, an extremely slow rate compared with other bacteria, which usually divide in less than an hour.[14] Since MTB has a cell wall but lacks a phospholipid outer membrane, it is classified as a Gram-positive bacterium. However, if a Gram stain is performed, MTB either stains very weakly Gram-positive or does not retain dye as a result of the high lipid and mycolic acid content of its cell wall.[15] MTB can withstand weak disinfectants and survive in a dry state for weeks. In nature, the bacterium can grow only within the cells of a host organism, but M. tuberculosis can be cultured in the laboratory.[16]
Using histological stains on expectorate samples from phlegm (also called sputum), scientists can identify MTB under a regular microscope. Since MTB retains certain stains after being treated with acidic solution, it is classified as an acid-fast bacillus (AFB).[1][15] The most common acid-fast staining technique, the Ziehl-Neelsen stain, dyes AFBs a bright red that stands out clearly against a blue background. Other ways to visualize AFBs include an auramine-rhodamine stain and fluorescent microscopy.
The M. tuberculosis complex includes four other TB-causing mycobacteria: M. bovis, M. africanum, M. canetti, and M. microti.[17] M. africanum is not widespread, but in parts of Africa it is a significant cause of tuberculosis.[18][19] M. bovis was once a common cause of tuberculosis, but the introduction of pasteurized milk has largely eliminated this as a public health problem in developed countries.[1][20] M. canetti is rare and seems to be limited to Africa, although a few cases have been seen in African emigrants.[21] M. microti is mostly seen in immunodeficient people, although it is possible that the prevalence of this pathogen has been underestimated.[22] Other known pathogenic mycobacteria include Mycobacterium leprae, Mycobacterium avium, and M. kansasii. The latter two are part of the nontuberculous mycobacteria (NTM) group. Nontuberculous mycobacteria cause neither TB nor leprosy, but they do cause pulmonary diseases resembling TB.[23]
There are a number factors that make people more susceptible to TB infections. Worldwide the most important of these is HIV with co-infection present in about 13% of cases.[6] This is a particular problem in Sub-Saharan Africa where rates of HIV are high.[24][25] Tuberculosis is closely linked to both overcrowding and malnutrition making it one of the principal diseases of poverty.[7] Chronic lung disease is a risk factor with smoking more than 20 cigarettes a day increasing the risk by two to four times[26] and silicosis increasing the risk about 30 fold.[27] Other disease states that increase the risk of developing tuberculosis include alcoholism[7] and diabetes mellitus (threefold increase).[28] Certain medications such as corticosteroids and Infliximab (an anti-αTNF monoclonal antibody) are becoming increasingly important risk factors, especially in the developed world.[7] There is also a genetic susceptibility[29] for which overall importance is still undefined.[7]
When people with active pulmonary TB cough, sneeze, speak, sing, or spit, they expel infectious aerosol droplets 0.5 to 5 µm in diameter. A single sneeze can release up to 40,000 droplets.[30] Each one of these droplets may transmit the disease, since the infectious dose of tuberculosis is very low and inhaling fewer than ten bacteria may cause an infection.[31]
People with prolonged, frequent, or intense contact are at particularly high risk of becoming infected, with an estimated 22% infection rate. A person with active but untreated tuberculosis can infect 10–15 other people per year.[3] Others at risk include people in areas where TB is common, people who inject illicit drugs, residents and employees of high-risk congregate settings, medically under-served and low-income populations, high-risk racial or ethnic minority populations, children exposed to adults in high-risk categories, those who are immunocompromised by conditions such as HIV/AIDS, people who take immunosuppressant drugs, and health care workers serving these high-risk clients.[32]
Transmission can only occur from people with active—not latent—TB.[1] The probability of transmission from one person to another depends upon the number of infectious droplets expelled by a carrier, the effectiveness of ventilation, the duration of exposure, and the virulence of the M. tuberculosis strain.[33] The chain of transmission can be broken by isolating people with active disease and starting effective anti-tuberculous therapy. After two weeks of such treatment, people with non-resistant active TB generally cease to be contagious. If someone does become infected, then it will take three to four weeks before the newly infected person can transmit the disease to others.[34]
About 90% of those infected with Mycobacterium tuberculosis have asymptomatic, latent TB infection (sometimes called LTBI), with only a 10% lifetime chance that a latent infection will progress to TB disease.[1] However, if untreated, the death rate for these active TB cases is more than 50%.[3]
TB infection begins when the mycobacteria reach the pulmonary alveoli, where they invade and replicate within the endosomes of alveolar macrophages.[1][35] The primary site of infection in the lungs is called the Ghon focus, and is generally located in either the upper part of the lower lobe, or the lower part of the upper lobe.[1] Simon foci may also be present. Bacteria are picked up by dendritic cells, which do not allow replication, although these cells can transport the bacilli to local (mediastinal) lymph nodes. Further spread is through the bloodstream to other tissues and organs where secondary TB lesions can develop in other parts of the lung (particularly the apex of the upper lobes), peripheral lymph nodes, kidneys, brain, and bone.[1][36] All parts of the body can be affected by the disease, though it rarely affects the heart, skeletal muscles, pancreas and thyroid.[37]
Tuberculosis is classified as one of the granulomatous inflammatory conditions. Macrophages, T lymphocytes, B lymphocytes, and fibroblasts are among the cells that aggregate to form granulomas, with lymphocytes surrounding the infected macrophages. The granuloma prevents dissemination of the mycobacteria and provides a local environment for interaction of cells of the immune system. Bacteria inside the granuloma can become dormant, resulting in a latent infection. Another feature of the granulomas of human tuberculosis is the development of abnormal cell death (necrosis) in the center of tubercles. To the naked eye this has the texture of soft white cheese and is termed caseous necrosis.[38]
If TB bacteria gain entry to the bloodstream from an area of damaged tissue they spread through the body and set up many foci of infection, all appearing as tiny white tubercles in the tissues. This severe form of TB disease is most common in infants and the elderly and is called miliary tuberculosis. People with this disseminated TB have a fatality rate near 100% if untreated. However, if treated early, the fatality rate is reduced to about 10%.[39]
In many people the infection waxes and wanes. Tissue destruction and necrosis are balanced by healing and fibrosis.[38] Affected tissue is replaced by scarring and cavities filled with cheese-like white necrotic material. During active disease, some of these cavities are joined to the air passages bronchi and this material can be coughed up. It contains living bacteria and can therefore spread the infection. Treatment with appropriate antibiotics kills bacteria and allows healing to take place. Upon cure, affected areas are eventually replaced by scar tissue.[38]
Tuberculosis is diagnosed definitively by identifying the causative organism (Mycobacterium tuberculosis) in a clinical sample (for example, sputum or pus). When this is not possible, a probable—although sometimes inconclusive[2]—diagnosis may be made using imaging (X-rays or scans), a tuberculin skin test (Mantoux test),[2] or a, Interferon Gamma Release Assay (IGRA).
The main problem with tuberculosis diagnosis is the difficulty in culturing this slow-growing organism in the laboratory (it may take 4 to 12 weeks for blood or sputum culture). A complete medical evaluation for TB must include a medical history, a physical examination, a chest X-ray, microbiological smears, and cultures. It may also include a tuberculin skin test, a serological test. The interpretation of the tuberculin skin test depends upon the person's risk factors for infection and progression to TB disease, such as exposure to other cases of TB or immunosuppression.[33]
New TB tests have been developed that are fast and accurate. These include polymerase chain reaction assays for the detection of bacterial DNA.[40] One such molecular diagnostics test gives results in 100 minutes and is currently being offered to 116 low- and middle-income countries at a discount with support from WHO and the Bill and Melinda Gates foundation.[41]
Another such test, which was approved by the FDA in 1996, is the amplified mycobacterium tuberculosis direct test (MTD, Gen-Probe). This test yields results in 2.5 to 3.5 hours, and it is highly sensitive and specific when used to test smears positive for acid-fast bacilli (AFB).[42]
Mantoux tuberculin skin tests are often used for routine screening of high risk individuals.[43] Currently, latent infection is diagnosed in a non-immunized person by a tuberculin skin test, which yields a delayed hypersensitivity type response to an extract made from M. tuberculosis.[1] Those immunized for TB or with past-cleared infection will respond with delayed hypersensitivity parallel to those currently in a state of infection, so the test must be used with caution, particularly with regard to persons from countries where TB immunization is common.[44] Tuberculin tests have the disadvantage of producing false negatives, especially when the person is co-morbid with sarcoidosis, Hodgkins lymphoma, malnutrition, or most notably active tuberculosis disease.[1] The newer interferon release assays (IGRAs) such as T-SPOT.TB and QuantiFERON-TB Gold In Tube overcome many of these problems. IGRAs are in vitro blood tests that are more specific than the skin test. IGRAs detect the release of interferon gamma in response to mycobacterial proteins such as ESAT-6.[45] These are not affected by immunization or environmental mycobacteria, so generate fewer false positive results.[46] There is also evidence that IGRAs are more sensitive than the skin test.[47]
Tuberculosis prevention and control efforts primarily rely on the vaccination of infants and the detection and appropriate treatment of active cases.[7] The World Health Organization has achieved some success with improved treatment success and a small decrease in case numbers.[7]
The only currently available vaccine as of 2011 is Bacillus Calmette-Guérin (BCG) which while effective against disseminated disease in childhood, confers inconsistent protection against pulmonary disease.[48] It is the most widely used vaccine worldwide with more than 90% of children vaccinated.[7] However the immunity that it induces, decreases after about ten years.[7] As tuberculosis is uncommon in most of Canada, the United Kingdom and the United States, BCG is only administered to people at high risk.[49][50][51] Part of the reason against the use of vaccine is that it makes the tuberculin skin test falsely positive and thus of no use in screening.[51] A number of new vaccines are in development.[7]
The World Health Organization (WHO) declared TB a global health emergency in 1993.[7] and in 2006 the Stop TB Partnership developed a Global Plan to Stop Tuberculosis that aims to save 14 million lives between its launch and 2015.[52] A number of targets that they have set are not likely to be achieved by 2015 due to the increase in HIV associated tuberculosis and multi-drug resistant tuberculosis.[7]
Treatment for TB uses antibiotics to kill the bacteria. Effective TB treatment is difficult, due to the unusual structure and chemical composition of the mycobacterial cell wall, which makes many antibiotics ineffective and hinders the entry of drugs.[53] The two antibiotics most commonly used are isoniazid and rifampicin and treatments can be prolonged.[33] Latent TB treatment usually uses a single antibiotic, while active TB disease is best treated with combinations of several antibiotics, to reduce the risk of the bacteria developing antibiotic resistance.[54] People with latent infections are treated to prevent them from progressing to active TB disease later in life.
The recommended treatment of new onset pulmonary tuberculosis as of 2010 is six months of a combination of antibiotic containing rifampin along isoniazid, pyrazinamide and ethambutol for the first two months and with just isoniazid for the last four months.[7] Where resistance to insoniazid is high ethambutol may be added for the last four months.[7]
If tuberculosis recurs, testing to determine what antibiotics it is sensitive to is important before determining treatment.[7] If multi-drug-resistant tuberculosis is detected, treatment with at least four effective antibiotics for 18-24 month is recommended.[7]
Primary resistance occurs in persons infected with a resistant strain of TB. A person with fully susceptible TB develops secondary resistance (acquired resistance) during TB therapy because of inadequate treatment, not taking the prescribed regimen appropriately, or using low-quality medication.[54] Drug-resistant TB is a public health issue in many developing countries, as treatment is longer and requires more expensive drugs. Multi-drug-resistant tuberculosis (MDR-TB) is defined as resistance to the two most effective first-line TB drugs: rifampicin and isoniazid. Extensively drug-resistant TB (XDR-TB) is also resistant to three or more of the six classes of second-line drugs.[55] Totally drug-resistant TB (TDR-TB), which was first observed in 2003 in Italy, but not widely reported until 2012, is resistant to all currently-used drugs.[56]
Progression from TB infection to TB disease occurs when the TB bacilli overcome the immune system defenses and begin to multiply. In primary TB disease—1–5% of cases—this occurs soon after infection.[1] However, in the majority of cases, a latent infection occurs that has no obvious symptoms.[1] These dormant bacilli can produce tuberculosis in 2–23% of these latent cases, often many years after infection.[57]
The risk of reactivation increases with immunosuppression, such as that caused by infection with HIV. In people co-infected with M. tuberculosis and HIV, the risk of reactivation increases to 10% per year.[1] Studies utilizing DNA fingerprinting of M. tuberculosis strains have shown that reinfection contributes more substantially to recurrent TB than previously thought,[58] with estimates that it might account for more than 50% in areas where TB is common.[59] The chance of death from a case of tuberculosis is about 4%.[7]
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no data
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10–25
25–50
50–75
75–100
100–250
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250–500
500–750
750–1000
1000–2000
2000–3000
≥ 3000
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Roughly a third of the world's population has been infected with M. tuberculosis, and new infections occur at a rate of one per second.[3] However, not all infections with M. tuberculosis cause TB disease and many infections are asymptomatic.[63] In 2007 there were an estimated 13.7 million chronic active cases,[5] and in 2010, 8.8 million new cases, and 1.45 million deaths, mostly in developing countries.[6] The absolute number of tuberculosis cases has been decreasing since 2005 and new cases since 2002.[6] China has achieved particularly dramatic progress, with an 80 percent decline in its TB mortality rate.[64] The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries test positive in tuberculin tests, while only 5–10% of the U.S. population test positive.[1] Tuberculosis is the world's greatest infectious killer of women of reproductive age and the leading cause of death among people with HIV/AIDS.[65] This is due to the fact that worldwide, women have a larger burden from poverty, ill-health, malnutrition and disease than men. Tuberculosis results in more deaths among women than all causes of maternal mortality combined, and more than 900 million women are infected with TB worldwide. It also kills more young people and adults than any other known infectious disease.[66]
The rise in HIV infections and the neglect of TB control programs have enabled a resurgence of tuberculosis.[67] The emergence of drug-resistant strains has also contributed to this new epidemic with, from 2000 to 2004, 20% of TB cases being resistant to standard treatments and 2% resistant to second-line drugs.[55] The rate at which new TB cases occur varies widely, even in neighbouring countries, apparently because of differences in health care systems.[68]
In 2007, the country with the highest estimated incidence rate of TB was Swaziland, with 1200 cases per 100,000 people. India had the largest total incidence, with an estimated 2.0 million new cases.[5] In developed countries, tuberculosis is less common and is mainly an urban disease. In the United Kingdom, the national average was 15 per 100,000 in 2007, and the highest incidence rates in Western Europe were 30 per 100,000 in Portugal and Spain. These rates compared with 98 per 100,000 in China and 48 per 100,000 in Brazil. In the United States, the overall tuberculosis case rate was 4 per 100,000 persons in 2007.[61] In Canada, tuberculosis is still endemic in some rural areas.[69]
The incidence of TB varies with age. In Africa, TB primarily affects adolescents and young adults.[70] However, in countries where TB has gone from high to low incidence, such as the United States, TB is mainly a disease of older people, or of the immunocompromised.[1][71]
Tuberculosis has been present in humans since antiquity.[7] The earliest unambiguous detection of Mycobacterium tuberculosis is in the remains of bison dated 17,000 years before the present.[72] However, whether tuberculosis originated in cattle and then transferred to humans, or diverged from a common ancestor, is currently unclear.[73] Although, there is evidence following a comparative genomic approach of MTBC in humans to MTBC in animals that suggests that humans did not acquire MTBC from animals during animal domestication as previously believed. Both strains of the tuberculosis bacteria are shown to share a common ancestor, which could have infected humans as early as the Neolithic transition.[74] Skeletal remains show prehistoric humans (4000 BCE) had TB, and researchers have found tubercular decay in the spines of Egyptian mummies dating from 3000-2400 BCE.[75] Phthisis is a Greek term for consumption; around 460 BCE, Hippocrates identified phthisis as the most widespread disease of the times involving coughing up blood and fever, which was almost always fatal.[76] Genetic studies suggest that TB was present in The Americas from about the year 100 CE.[77]
Before the Industrial Revolution, folklore often associated tuberculosis with vampires. When one member of a family died from it, the other members that were infected would lose their health slowly. People believed that this was caused by the original victim draining the life from the other family members.[78]
Although it was established that the pulmonary form was associated with 'tubercles' by Dr Richard Morton in 1689,[79][80] due to the variety of its symptoms, TB was not identified as a single disease until the 1820s and was not named 'tuberculosis' until 1839 by J. L. Schönlein.[81] During the years 1838–1845, Dr. John Croghan, the owner of Mammoth Cave, brought a number of tuberculosis sufferers 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.[82] Hermann Brehmer opened the first TB sanatorium in 1859 in Sokołowsko, Poland.[83]
The bacillus causing tuberculosis, Mycobacterium 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.[84] Koch did not believe that bovine (cattle) and human tuberculosis were similar, which delayed the recognition of infected milk as a source of infection. Later, this source was eliminated by the pasteurization process. 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 as a test for pre-symptomatic tuberculosis.[85]
Albert Calmette and Camille Guerin achieved the first genuine success in immunizing against tuberculosis in 1906, using attenuated bovine-strain tuberculosis. It was called 'BCG' (Bacillus of Calmette and Guerin). The BCG vaccine was first used on humans in 1921 in France,[86] but it wasn't until after World War II that BCG received widespread acceptance in the USA, Great Britain, and Germany.[87]
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 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 resembled prisons; the sanatoria for the middle and upper classes offered excellent care and constant medical attention.[83] Whatever the purported benefits of the fresh air and labor in the sanatoria, even under the best conditions, 50% of those who entered were dead within five years (1916).[83]
The promotion of Christmas Seals began in Denmark during 1904 as a way to raise money for tuberculosis programs. It expanded to the United States and Canada in 1907–1908 to help the National Tuberculosis Association (later called the American Lung Association).
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 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.[88]
It was not until 1946 with the development of the antibiotic streptomycin that effective treatment and cure became possible. Prior to the introduction of this drug, the only treatment besides sanatoria were surgical interventions, including the pneumothorax technique—collapsing an infected lung to "rest" it and allow lesions to heal—a technique that was of little benefit and was largely discontinued by the 1950s.[89] The emergence of multidrug-resistant TB has again introduced surgery as part of the treatment for these infections. Here, surgical removal of chest cavities will reduce the number of bacteria in the lungs, as well as increasing the exposure of the remaining bacteria to drugs in the bloodstream, and is therefore thought to increase the effectiveness of the chemotherapy.[90]
Hopes of completely eliminating the disease were dashed following the rise of drug-resistant strains in the 1980s. For example, tuberculosis cases in Britain, numbering around 50,000 in 1955, had fallen to around 5,500 in 1987, but in 2000 there were over 7,000 confirmed cases.[citation needed] Due to the elimination of public health facilities in New York and the emergence of HIV, there was a resurgence in the late 1980s.[91] The number of those failing to complete their course of drugs is high. NY had to cope with more than 20,000 "unnecessary" TB-patients with multidrug-resistant strains (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.[92]
Tuberculosis can be carried by mammals; domesticated species, such as cats and dogs, are generally free of tuberculosis, but wild animals may be carriers. In some places, regulations aiming to prevent the spread of TB restrict the ownership of novelty pets; for example, the U.S. state of California forbids the ownership of pet gerbils.[93]
Mycobacterium bovis causes TB in cattle. An effort to eradicate bovine tuberculosis from the cattle and deer herds of New Zealand is under way. It has been found that herd infection is more likely in areas where infected vector species such as Australian brush-tailed possums come into contact with domestic livestock at farm/bush borders.[94] Controlling the vectors through possum eradication and monitoring the level of disease in livestock herds through regular surveillance are seen as a "two-pronged" approach to ridding New Zealand of the disease.
In both the Republic of Ireland and Northern Ireland, badgers have been identified as a vector species for the transmission of bovine tuberculosis. As a result, the government in both regions has mounted an active campaign of eradication of the species in an effort to reduce the incidence of the disease. Badgers have been culled primarily by snaring and gassing. It remains a contentious issue, with proponents and opponents of the scheme citing their own studies to support their position.[95][96][97]
Several new vaccines to prevent TB infection are being developed, among others by Aeras and TBVI. The first recombinant tuberculosis vaccine, Mtb72F, entered clinical trials in the United States in 2004, sponsored by the National Institute of Allergy and Infectious Diseases (NIAID).[98][99] A 2005 study showed that a DNA TB vaccine given with conventional chemotherapy can accelerate the disappearance of bacteria as well as protect against re-infection in mice; it may take four to five years to be available in humans.[100] Another TB vaccine, MVA85A, is currently in phase II trials in South Africa,[101] and is based on a genetically modified vaccinia virus. Many other strategies are also being used to develop novel vaccines,[102] including both subunit vaccines (fusion molecules composed of two recombinant proteins delivered in an adjuvant) such as Hybrid-1, HyVac4, or M72, and recombinant adenoviruses such as Ad35.[103][104][105][106] Some of these vaccines can be effectively administered without needles, making them preferable for areas where HIV is common.[107] All of these vaccines have been successfully tested in humans and are now in extended testing in TB-endemic regions. To encourage further discovery, researchers and policymakers are promoting new economic models of vaccine development including prizes, tax incentives, and advance market commitments.[108][109]
An experimental vaccine, with positive results in mouse models, may be effective not only in preventing infection, but also in eradicating the infection once it has been established.[110] A tuberculosis vaccine aimed at sterile Mtb eradication should be able to target latent Mtb as well as Mtb that causes early-stage tuberculosis.[111] The vaccine is a combination of antigens Ag85B and ESAT-6 as well as the protein Rv2660c. Ag85B and ESAT-6 together form the vaccine Hybrid-1, while Rv2660c is a protein that is expressed even in late-stage infections, when protein transcription is generally reduced. The novel combination of Ag85B, ESAT-6, and Rv2660c allows for both short- and long-term protection as a result of the continued expression of target proteins. The new vaccine, currently referred to as H56, works by promoting a polyfunctional CD4+ T cell response against tuberculosis protein components.[110] Phase I clinical trials began in Cape Town, South Africa, in December 2011.[112]
A number of groups including the Mycobacterium Tuberculosis Structural Genomics Consortium and The Tuberculosis Vaccine Initiative (TBVI) are involved with research.
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Translations:
Tuberculosis |
Dansk (Danish)
n. - tuberkulose
Nederlands (Dutch)
tuberculose
Français (French)
n. - tuberculose
Deutsch (German)
n. - Tuberkulose
Ελληνική (Greek)
n. - (παθολ.) φυματίωση, φθίση (κν. χτικιό)
Italiano (Italian)
tubercolosi
Português (Portuguese)
n. - tuberculose
Español (Spanish)
n. - tuberculosis
Svenska (Swedish)
n. - tuberkulos (med.)
中文（简体）(Chinese (Simplified))
肺结核
中文（繁體）(Chinese (Traditional))
n. - 肺結核
العربيه (Arabic)
(الاسم) مرض السل
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