Tuberculosis

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Tuberculosis
Classification & external resources

Chest X-ray of a patient suffering from

tuberculosis

ICD-10

A15.-A19.

ICD-9

010-018

OMIM

607948

DiseasesDB 8515
MedlinePlus 000077 000624
eMedicine med/2324 emerg/618
radio/411
MeSH

C01.252.410.040.552.846

Tuberculosis (abbreviated as TB for tubercle bacillus or Tuberculosis) is a common and

deadly infectious disease caused by mycobacteria, mainly Mycobacterium tuberculosis.
Tuberculosis most commonly attacks the lungs (as pulmonary TB) but can also affect the
central nervous system, the lymphatic system, the circulatory system, the genitourinary
system, bones, joints and even the skin. Other mycobacteria such as Mycobacterium
bovis, Mycobacterium africanum, Mycobacterium canetti, and Mycobacterium microti
can also cause tuberculosis, but these species do not usually infect healthy adults.[1]

Over one-third of the world's population has been exposed to the TB bacterium, and new
infections occur at a rate of one per second.[2] Not everyone infected develops the fullblown disease; asymptomatic, latent TB infection is most common. However, one in ten
latent infections will progress to active TB disease, which, if left untreated, kills more
than half of its victims.
In 2004, mortality and morbidity statistics included 14.6 million chronic active TB cases,
8.9 million new cases, and 1.6 million deaths, mostly in developing countries.[2] In
addition, a rising number of people in the developed world are contracting tuberculosis
because their immune systems are compromised by immunosuppressive drugs, substance
abuse, or HIV/AIDS.
The rise in HIV infections and the neglect of TB control programs have enabled a
resurgence of tuberculosis.[3] 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.[4] TB incidence varies widely,
even in neighboring countries, apparently because of differences in health care systems.[5]
The World Health Organization declared TB a global health emergency in 1993, and the
Stop TB Partnership developed a Global Plan to Stop Tuberculosis that aims to save 14
million lives between 2006 and 2015.[6]

Contents
[hide]

1 Other names
2 Symptoms
3 Bacterial species
o 3.1 Evolution
4 Transmission
5 Pathogenesis
6 Diagnosis
7 Progression
8 Treatment
9 Prevention
o 9.1 Vaccines
10 Epidemiology
11 History
o 11.1 Folklore
o 11.2 Study and treatment
12 Infection of other animals
13 See also
14 References
15 Further reading

16 External links

Other names
In the past, tuberculosis was called consumption, because it seemed to consume people
from within, with a bloody cough, fever, pallor, and long relentless wasting. Other names
included phthisis (Greek for consumption) and phthisis pulmonalis; scrofula (in
adults), affecting the lymphatic system and resulting in swollen neck glands; tabes
mesenterica, TB of the abdomen and lupus vulgaris, TB of the skin; wasting disease;
white plague, because sufferers appear markedly pale; king's evil, because it was
believed that a king's touch would heal scrofula; and Pott's disease, or gibbus of the
spine and joints.[7][8] Miliary tuberculosis now commonly known as disseminated TB
occurs when the infection invades the circulatory system resulting in lesions which have
the appearance of millet seeds on X-ray.[7][9]

Symptoms
Further information: Tuberculosis classification
When the disease becomes active, 75% of the cases are pulmonary TB. Symptoms
include chest pain, coughing up blood, and a productive, prolonged cough for more than
three weeks. Systemic symptoms include fever, chills, night sweats, appetite loss, weight
loss, pallor, and often a tendency to fatigue very easily.[2]
In the other 25% of active cases, the infection moves from the lungs, causing other kinds
of TB more common in immunosuppressed persons and young children. Extrapulmonary
infection sites include the pleura, the central nervous system in meningitis, the lymphatic
system in scrofula of the neck, the genitourinary system in urogenital tuberculosis, and
bones and joints in Pott's disease of the spine. An especially serious form is disseminated
TB, more commonly known as miliary tuberculosis. Although extrapulmonary TB is not
contagious, it may co-exist with pulmonary TB, which is contagious.[10]

Bacterial species
Main article: Mycobacterium tuberculosis

Scanning electron micrograph of Mycobacterium tuberculosis

The primary cause of TB , Mycobacterium tuberculosis (M. TB), is an aerobic bacterium
that divides every 16 to 20 hours, an extremely slow rate compared with other bacteria,
which usually divide in less than an hour.[11] (For example, one of the fastest-growing
bacteria is a strain of E. coli that can divide roughly every 20 minutes.) 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 Grampositive or does not retain dye due to the high lipid & mycolic acid content of its cell
wall.[12] MTB is a small rod-like bacillus that 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 vitro.[13]
Using certain histological techniques 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).[12] The most common 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 3 other TB-causing mycobacteria: M. bovis, M.
africanum and M. microti. The first two only very rarely cause disease in
immunocompetent people. On the other hand, although M. microti is not usually
pathogenic, it is possible that the prevalence of M. microti infections has been
underestimated.[14]
Other known pathogenic mycobacteria include Mycobacterium leprae, Mycobacterium
avium and M. kansasii. The last two are part of the nontuberculous mycobacteria (NTM)
group. Nontuberculous mycobacteria cause neither TB nor leprosy, but they do cause
pulmonary diseases resembling TB.[15]

Evolution
During its evolution, M. tuberculosis has lost numerous coding and non-coding regions in
its genome, losses that can be used to distinguish between strains of the bacteria. The
implication is that M. tuberculosis strains differ geographically, so their genetic
differences can be used to track the origins and movement of each strain.[16]

Transmission
Further information: Transmission (medicine)
When people suffering from active pulmonary TB cough, sneeze, speak, kiss, or spit,
they expel infectious aerosol droplets 0.5 to 5 m in diameter. A single sneeze, for
instance, can release up to 40,000 droplets.[17] Each one of these droplets may transmit the

disease, since the infectious dose of tuberculosis is very low and the inhalation of just a
single bacterium can cause a new infection.[18]

Tuberculosis is spread by aerosols created by coughing or sneezing.

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 1015 other people per year.[2] Others at risk include
people in areas where TB is common, people who inject illicit drugs (especially when
sharing needles), 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, patients
immunocompromised by conditions such as HIV/AIDS, people who take
immunosuppressant drugs, and health care workers serving these high-risk clients.[19]
Transmission can only occur from people with activenot latentTB. 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.[10] The chain of transmission can therefore
be broken by isolating patients 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.[20]

Pathogenesis
Mycobacterium tuberculosis (stained red) in sputum
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. However, if untreated, the death rate for these
active TB cases is more than 50%.[21]
TB infection begins when the mycobacteria reach the pulmonary alveoli, where they
invade and replicate within alveolar macrophages.[22] The primary site of infection in the

lungs is called the Ghon focus. 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 the more distant tissues and
organs where secondary TB lesions can develop in lung apices, peripheral lymph nodes,
kidneys, brain, and bone.[23] All parts of the body can be affected by the disease, though it
rarely affects the heart, skeletal muscles, pancreas and thyroid.[24]
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 a granuloma, with lymphocytes surrounding the infected macrophages.
The granuloma functions not only to prevent dissemination of the mycobacteria, but also
provides a local environment for communication of cells of the immune system. Within
the granuloma, T lymphocytes (CD4+) secrete cytokines such as interferon gamma,
which activates macrophages to destroy the bacteria with which they are infected.[25] T
lymphocytes (CD8+) can also directly kill infected cells.[22]
Importantly, bacteria are not always eliminated within the granuloma, but can become
dormant, resulting in a latent infection. Another feature of the granulomas of human
tuberculosis is the development of cell death, also called necrosis, in the center of
tubercles. To the naked eye this has the texture of soft white cheese and was termed
caseous necrosis.[26]
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. Patients with this disseminated TB have a fatality rate
of approximately 20%, even with intensive treatment.[27]
In many patients the infection waxes and wanes. Tissue destruction and necrosis are
balanced by healing and fibrosis.[26] 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 pass on infection. Treatment with appropriate
antibiotics kills bacteria and allows healing to take place. Upon cure, affected areas are
eventually replaced by scar tissue.[26]

Diagnosis
For more details on this topic, see Tuberculosis diagnosis.

Mantoux tuberculin skin test

Tuberculosis can be a difficult disease to diagnose, due mainly to the difficulty in
culturing this slow-growing organism in the laboratory. A complete medical evaluation
for TB must include a medical history, a chest X-ray, and a physical examination.
Tuberculosis radiology is used in the diagnosis of TB. It may also include a tuberculin
skin test, a serological test, microbiological smears and cultures. 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.[10]
Currently, latent infection is diagnosed in a non-immunized person by a tuberculin skin
test, which yields a delayed hypersensitivity type response to purified protein derivatives
of M. tuberculosis. Those immunized for TB or with past-cleared infection will respond
with delayed hypersensitivity parallel to those currently in a state of infection and thus
the test must be used with caution, particularly with regard to persons from countries
where TB immunization is common.[28] New TB tests are being developed that offer the
hope of cheap, fast and more accurate TB testing. These use polymerase chain reaction
detection of bacterial DNA and antibody assays to detect the release of interferon gamma
in response to mycobacteria.[29] Rapid and inexpensive diagnosis will be particularly
valuable in the developing world.

Progression
Progression from TB infection to TB disease occurs when the TB bacilli overcome the
immune system defenses and begin to multiply. In primary TB disease1 to 5% of cases
this occurs soon after infection. However, in the majority of cases, a latent infection
occurs that has no obvious symptoms. These dormant bacilli can produce tuberculosis in
2 to 23% of these latent cases, often many years after infection.[30] The risk of reactivation
increases with immunosuppression, such as that caused by infection with HIV. In patients
co-infected with M. tuberculosis and HIV, the risk of reactivation increases to 10% per
year.[21]

Other conditions that increase risk include drug injection, mainly due to the lifestyle of
IV drug users; recent TB infection or a history of inadequately treated TB; chest X-ray
suggestive of previous TB, showing fibrotic lesions and nodules; diabetes mellitus;
silicosis; prolonged corticosteroid therapy and other immunosuppressive therapy; head
and neck cancers; hematologic and reticuloendothelial diseases, such as leukemia and
Hodgkin's disease; end-stage kidney disease; intestinal bypass or gastrectomy; chronic
malabsorption syndromes; or low body weight.[10]
Twin studies in the 1950's showed that the course of TB infection was highly dependent
on the genetics of the patient. At that time, it was rare that one identical twin would die
and the other live.[31]
Some drugs, including rheumatoid arthritis drugs that work by blocking tumor necrosis
factor-alpha (an inflammation-causing cytokine), raise the risk of activating a latent
infection due to the importance of this cytokine in the immune defense against TB.[32]

Treatment
For more details on this topic, see Tuberculosis treatment.
Treatment for TB uses antibiotics to kill the bacteria. The two antibiotics most commonly
used are rifampicin and isoniazid. However, instead of the short course of antibiotics
typically used to cure other bacterial infections, TB requires much longer periods of
treatment (around 6 to 12 months) to entirely eliminate mycobacteria from the body.[10]
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.[33] People with these latent infections are treated to
prevent them from progressing to active TB disease later in life. However, treatment
using Rifampin and Pyrazinamide is not risk-free. The Centers for Disease Control and
Prevention (CDC) notified healthcare professionals of revised recommendations against
the use of rifampin plus pyrazinamide for treatment of latent tuberculosis infection, due
to high rates of hospitalization and death from liver injury associated with the combined
use of these drugs.[34]
Drug resistant tuberculosis is transmitted in the same way as regular TB. Primary
resistance occurs in persons who are infected with a resistant strain of TB. A patient 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.[33] Drug-resistant TB is a public health issue in many
developing countries, as treatment is longer and requires more expensive drugs. Multidrug resistant TB (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.[4]
In ancient times, available treatments focused more on dietary parameters. Pliny the Elder
described several methods in his Natural History: "wolf's liver taken in thin wine, the lard

of a sow that has been fed upon grass, or the flesh of a she-ass taken in broth".[35] While
these particular remedies haven't been tested scientifically, it has been demonstrated that
malnourished mice receiving a 2% protein diet suffer far higher mortality from
tuberculosis than those receiving 20% protein receiving the same infectious challenge
dose, and the progressively fatal course of the illness could be reversed by restoring the
mice to the normal diet.[36] Moreover, statistics for immigrants in South London reveal an
8.5 fold increased risk of tuberculosis in (primarily Hindu Asian) lacto vegetarians, who
frequently suffer protein malnutrition, compared to those of similar cultural backgrounds
who ate meat and fish daily.[37]

Prevention
TB prevention and control takes two parallel approaches. In the first, people with TB and
their contacts are identified and then treated. Identification of infections often involves
testing high-risk groups for TB. In the second approach, children are vaccinated to protect
them from TB. Unfortunately, no vaccine is available that provides reliable protection for
adults. However, in tropical areas where the incidence of atypical mycobacteria is high,
exposure to nontuberculous mycobacteria gives some protection against TB.[38]

Vaccines
Many countries use BCG vaccine as part of their TB control programs, especially for
infants. This was the first vaccine for TB and developed at the Pasteur Institute in France
between 1905 and 1921.[39] However, mass vaccination with BCG did not start until after
World War II.[40] The protective efficacy of BCG for preventing serious forms of TB (e.g.
meningitis) in children is greater than 80%; its protective efficacy for preventing
pulmonary TB in adolescents and adults is variable, ranging from 0 to 80%.[41]
In South Africa, the country with the highest prevalence of TB, BCG is given to all
children under the age of three.[42] However, the effectiveness of BCG is lower in areas
where mycobacteria are less prevalent, therefore BCG is not given to the entire
population in these countries. In the USA, for example, BCG vaccine is not
recommended except for people who meet specific criteria:[10]

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

Several new vaccines to prevent TB infection are being developed. 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).[43] 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.[44] A very promising TB vaccine, MVA85A, is
currently in phase II trials in South Africa by a group led by Oxford University,[45] and is
based on a genetically modified vaccinia virus. Because of the limitations of current
vaccines, researchers and policymakers are promoting new economic models of vaccine
development including prizes, tax incentives and advance market commitments.[46][47]

Epidemiology
Annual number of new reported TB cases. Data from WHO.[48]
World TB incidence. Cases per 100,000; Red = >300, orange = 200300; yellow = 100
200; green 50100 and grey <50. Data from WHO, 2005.[48]
According to the World Health Organization (WHO), nearly 2 billion peopleonethird
of the world's populationhave been exposed to the tuberculosis pathogen.[49] Annually,
8 million people become ill with tuberculosis, and 2 million people die from the disease
worldwide.[50] In 2004, around 14.6 million people had active TB disease with 9 million
new cases. The annual incidence rate varies from 356 per 100,000 in Africa to 41 per
100,000 in the Americas.[2] Tuberculosis is the world's greatest infectious killer of women
of reproductive age and the leading cause of death among people with HIV/AIDS.[51]
In 2005, the country with the highest estimated incidence of TB was Swaziland, with
1262 cases per 100,000 people. India has the largest number of infections, with over 1.8
million cases. [52] In developed countries, tuberculosis is less common and is mainly an
urban disease. In the United Kingdom, TB incidences range from 40 per 100,000 in
London to less than 5 per 100,000 in the rural South West of England;[53] the national
average is 13 per 100,000. The highest rates in Western Europe are in Portugal (42 per
100,000) and Spain (20 per 100,000). These rates compare with 113 per 100,000 in China
and 64 per 100,000 in Brazil. In the United States, the overall tuberculosis case rate was
4.9 per 100,000 persons in 2004.[50]
The incidence of TB varies with age. In Africa, TB primarily affects adolescents and
young adults.[54] 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.[55]
There are a number of known factors that make people more susceptible to TB infection:
worldwide the most important of these is HIV. Co-infection with HIV is a particular
problem in Sub-Saharan Africa, due to the high incidence of HIV in these countries.[48][56]
Smoking more than 20 cigarettes a day also increases the risk of TB by two- to fourtimes.[57][58] Diabetes mellitus is also an important risk factor that is growing in
importance in developing countries.[59]

History

Tubercular decay has been found in the spines of Egyptian mummies. Pictured: Egyptian
mummy in the British Museum
Tuberculosis has been present in humans since antiquity. The earliest unambiguous
detection of Mycobacterium tuberculosis is in the remains of bison dated 18,000 years
before the present.[60] However, whether tuberculosis originated in cattle and then
transferred to humans, or diverged from a common ancestor, is currently unclear.[61]
Skeletal remains show prehistoric humans (4000 BC) had TB, and tubercular decay has
been found in the spines of mummies from 3000-2400 BC.[62] Phthisis is a Greek term for
tuberculosis; around 460 BC, Hippocrates identified phthisis as the most widespread
disease of the times involving coughing up blood and fever, which was almost always
fatal.[63] Genetic studies suggest that TB was present in South America for about 2,000
years.[64] In South America, the earliest evidence of tuberculosis is associated with the
Paracas-Caverna culture (circa 750 BC to circa 100 AD).[65]

Folklore
Before the Industrial Revolution, tuberculosis may sometimes have been regarded as
vampirism. 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. Furthermore, people who
had TB exhibited symptoms similar to what people considered to be vampire traits.
People with TB often have symptoms such as red, swollen eyes (which also creates a
sensitivity to bright light), pale skin and coughing blood, suggesting the idea that the only
way for the afflicted to replenish this loss of blood was by sucking blood.[66] Another folk
belief attributed it to being forced, nightly, to attend fairy revels, so that the victim wasted
away owing to lack of rest; this belief was most common when a strong connection was
seen between the fairies and the dead.[67] Similarly, but less commonly, it was attributed to
the victims being "hagridden"being transformed into horses by witches (hags) to travel
to their nightly meetings, again resulting in a lack of rest.[67]

TB was romanticized in the nineteenth century. Many at the time believed TB produced
feelings of euphoria referred to as "Spes phthisica" or "hope of the consumptive". It was
believed that TB sufferers who were artists had bursts of creativity as the disease
progressed. It was also believed that TB sufferers acquired a final burst of energy just
before they died which made women more beautiful and men more creative.[68]

Study and treatment

The study of tuberculosis dates back to The Canon of Medicine written by Ibn Sina
(Avicenna) in the 1020s. He was the first physician to identify pulmonary tuberculosis as
a contagious disease, the first to recognise the association with diabetes, and the first to
suggest that it could spread through contact with soil and water.[69][70] He developed the
method of quarantine in order to limit the spread of tuberculosis.[71]
Although it was established that the pulmonary form was associated with 'tubercles' by
Dr Richard Morton in 1689,[72][73] 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. Schnlein.[74] During the years 18381845, 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.[75] The first TB sanatorium opened in 1859 in Grbersdorf, Germany (today
Sokoowsko, Poland) by Hermann Brehmer.[76]
In regard to this claim, The Times for January 15, 1859, page 5, column 5, carries an
advertisement seeking funds for the Bournemouth Sanatorium for Consumption, referring
to the balance sheet for the past year, and offering an annual report to prospective donors,
implying that this sanatorium was in existence at least in 1858.

Dr. Robert Koch discovered the tuberculosis bacilli.

The bacillus causing tuberculosis, Mycobacterium tuberculosis, was identified and

described on March 24, 1882 by Robert Koch. He received the Nobel Prize in physiology
or medicine in 1905 for this discovery.[77] 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 presymptomatic tuberculosis.[78]
The first genuine success in immunizing against tuberculosis was developed from
attenuated bovine-strain tuberculosis by Albert Calmette and Camille Guerin in 1906. It
was called 'BCG' (Bacillus of Calmette and Guerin). The BCG vaccine was first used on
humans in 1921 in France,[39] but it wasn't until after World War II that BCG received
widespread acceptance in the USA, Great Britain, and Germany.[40]
Tuberculosis, or 'consumption' as it was commonly known, 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. In the 20th century, tuberculosis killed an
estimated 100 million people.[79] 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.[76] 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).[76]

Public health campaigns tried to halt the spread of TB

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
08 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.[80]
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
techniquecollapsing an infected lung to "rest" it and allow lesions to heala technique
that was of little benefit and was largely discontinued by the 1950s.[81] 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.
[82]

Hopes that the disease could be completely eliminated have been dashed since the rise of
drug-resistant strains in the 1980s. For example, tuberculosis cases in Britain, numbering
around 117,000 in 1913, had fallen to around 5,000 in 1987, but cases rose again,
reaching 6,300 in 2000 and 7,600 cases in 2005.[83] Due to the elimination of public
health facilities in New York and the emergence of HIV, there was a resurgence in the late
1980s.[84] 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.[85]

Infection of other animals

Main article: Mycobacterium bovis
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.[86]

Mycobacterium bovis causes TB in cattle. An effort to eradicate bovine tuberculosis from

the cattle and deer herds of New Zealand is underway. It has been found that herd
infection is more likely in areas where infected vector species such as Australian brushtailed possums come into contact with domestic livestock at farm/bush borders.[87]
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 the Republic of Ireland and the United Kingdom, badgers have been identified as one
vector species for the transmission of bovine tuberculosis. As a result, governments have
come under pressure from some quarters, primarily dairy farmers, to mount an active
campaign of eradication of badgers in certain areas with the purpose of reducing the
incidence of bovine TB. The UK government has not committed itself on the issue, not
least because it fears public opinion: badgers are a protected species. The effectiveness of
culling on the incidence of TB in cattle is a contentious issue, with proponents and
opponents citing their own studies to support their position.[88][89][90] A 9-year scientific
study by an Independent Study Group of the likely efficacy of badger culling reported on
18 June 2007 that it was unlikely to be effective and could actually increase the spread of
TB. The Independent Study Group was chaired by Sir John Bourne and included two
statisticians, Professor Cristl Donnelly and Sir David Cox, the most distinguished
statistician in the United Kingdom. Donnelly and Cox produced a sophisticated stochastic
model of the badger population which was used to make detailed quantitative predictions
about the effects of various policies. The recommendations of the Bourne report[91] came
as a surprise to Ministers. The UK Government's Chief Scientific Adviser, Sir David
King convened a committee to re-examine the Bourne report. King's committee produced
a report on 30th July, only one month after the publication of Bourne's 9-year study,
whose conclusions flatly contradicted those of the Bourne report and recommended
badger culling. [92]. The King committee did not include any statisticians and did not make
use of the Donnelly & Cox statistical model. As a result, the issue of badger culling
remains hugely controversial in the United Kingdom.

See also

2007 tuberculosis scare

Abreugraphy
ATC code J04 Drugs for treatment of TB
Buruli ulcer and leprosy: other diseases caused by mycobacteria
Latent tuberculosis
List of tuberculosis victims
Mycobacterium Tuberculosis Structural Genomics Consortium
National Center for HIV, STD, and TB Prevention
Nontuberculous mycobacteria
Overcrowding
Philip D'Arcy Hart
Tuberculosis in history and art
UNITAID

Nosocomial infection

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Further reading

Blumberg HM, Leonard MK, Jasmer RM (2005). "Update on the treatment of

tuberculosis and latent tuberculosis infection". JAMA 293 (22): 2776-84.
doi:10.1001/jama.293.22.2776. PMID 15941808.
Dormandy, Thomas (2000). The White Death. New York: New York University Press.
ISBN 0814719279.
Joint Tuberculosis Committee of the British Thoracic Society (2000). "Control and
prevention of tuberculosis in the United Kingdom: code of practice 2000.". Thorax 55
(11): 887-901. PMID 11050256.
Kidder, Tracy (2004). Mountains Beyond Mountains. New York: Random House Trade
Paperbacks. ISBN 0812973011. A nonfiction account of treating TB in Haiti, Peru,
Russia, and elsewhere.
Lawlor, Clark (2007). Consumption and Literature. Basingstoke: Palgrave Macmillan.
ISBN 0230020038.
Nemery B, Yew WW, Albert R, et al (2005). "Tuberculosis, nontuberculous lung
infection, pleural disorders, pulmonary function, respiratory muscles, occupational lung

disease, pulmonary infections, and social issues in AJRCCM in 2004". Am. J. Respir.
Crit. Care Med. 171 (6): 554-62. doi:10.1164/rccm.2412009. PMID 15753485.
Ryan, Frank (1993), The Forgotten Plague: How the Battle Against Tuberculosis Was
Won and Lost, Boston, MA: Little, Brown and Company, ISBN 0-316-76380-2. First
published in the United Kingdom as Tuberculosis: The Greatest Story Never Told.
Walton D, Farmer P (2000). "MSJAMA: the new white plague". JAMA 284 (21): 2789.
PMID 11105192.

External links
Wikimedia Commons has media related to:
Tuberculosis
Tuberculosis at the Open Directory Project
Centers for Disease Control and Prevention (CDC), Division of Tuberculosis
Elimination. Core Curriculum on Tuberculosis: What the Clinician Should Know.
4th edition (2000). Updated Aug 2003.
(CDC) - Division of Tuberculosis Elimination News and updates.
(CDC) - Questions and Answers About TB, 2007.
Health Protection Agency, England - [4]
BioHealthBase Bioinformatics Resource Center. Database of Mycobacterium
tuberculosis genome sequences and related information.
Kaiser Family Foundation. Tuberculosis. Globalhealthfacts.org.
The Nobel Prize Website. Tuberculosis Educational Game
United States Agency for International Development (USAID). The Tuberculosis
Coalition for Technical Assistance (TBCTA).
World Health Organization (WHO). Tuberculosis.
Tuberculosis and HIV: HIV InSite Knowledge Base chapter and related resources.
[hide]
vde

Bacterial diseases (primarily A00-A79, 001-041,080-109)

Clostridium (Pseudomembranous colitis, Botulism, Tetanus, Gas
gangrene) - Streptococcus A and B (Scarlet fever, Erysipelas) G+/Firmicutes
Staphylococcus (Toxic shock syndrome) - Bacilli (Anthrax,
Listeriosis)
Mycobacterium: Tuberculosis (Ghon focus, Ghon's complex,
Tuberculous meningitis, Pott's disease, Scrofula, Bazin disease,
Lupus vulgaris, Miliary tuberculosis) - Leprosy - Lady Windermere
G+/Actinobacteria
syndrome - Buruli ulcer Actinomycetales: Actinomycosis - Nocardiosis - Diphtheria Erythrasma
Syphilis (Bejel) - Yaws - Pinta - Relapsing fever - Noma - Trench
G-/Spirochetal
mouth - Lyme disease - Rat-bite fever (Sodoku) - Leptospirosis

Chlamydophila (Psittacosis) - Chlamydia (Chlamydia,

Lymphogranuloma venereum, Trachoma)
Rickettsioses (Typhus, Scrub typhus, Rocky Mountain spotted
fever, Boutonneuse fever, Q fever, Trench fever, Rickettsialpox) G-/ Proteobacteria
Brucellosis - Cat scratch fever
Bartonellosis (Bacillary angiomatosis)
Salmonella (Typhoid fever, Paratyphoid fever, Salmonellosis) other intestinal (Cholera, Shigellosis) - Zoonotic (Bubonic plague,
Tularemia, Glanders, Melioidosis, Pasteurellosis) - Other: Pertussis
G-/& Proteobacteria
- Meningococcus (Meningococcal disease, WaterhouseFriderichsen syndrome) - Legionellosis - Brazilian purpuric fever Chancroid - Donovanosis - Gonorrhea
Retrieved from "http://en.wikipedia.org/wiki/Tuberculosis"
Categories: Deaths by tuberculosis | Bacterial diseases | Pulmonology | Tuberculosis |
Health problems in India | Health in Africa
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