Tuberculosis
(TB)
Tuberculosis a deadly disease, is on the rise and is
revisiting both the developed and developing world. Globally, it is the
leading cause of deaths resulting from a single infectious disease.
Currently, it kills three million Tuberculosis, a sometimes crippling and people
a year and, if the present trend continues, it is likely to claim more than 30
million lives within the next decade. Recent increases in migration have
rapidly mixed infected with uninfected communities and contributed to the spread
of the disease.
WHAT
IS TUBERCULOSIS?
Tuberculosis is an infectious disease caused by the microorganism Mycobacterium
tuberculosis. It can affect several organs of the human body, including
the brain, the kidneys and the bones; but most commonly it affects the lungs
(Pulmonary Tuberculosis). The first stage of the infection usually lasts
for several months. During this period, the body's natural defenses
(immune system) resist the disease, and most or all of the bacteria are walled
in by a fibrous capsule that develops around the area. Before the initial
attack is over, a few bacteria may escape into the bloodstream and be carried
elsewhere in the body, where they are again walled in. In many cases, the
disease never develops beyond this stage - and is referred to as TB infection.
If the immune system fails to stop the infection and it is left untreated, the
disease progresses to the second stage, active disease. There, the germ
multiplies rapidly and destroys the tissues of the lungs (or the other affected
organ). In some cases, the disease, although halted at first, flares up
after a latent period. Sometimes, the latent period is many years, and the
bacteria become active when the opportunity presents itself, especially when
immunity is low.
The second stage of the disease is manifested by destruction
or "consumption" of the tissues of the affected organ. When the
lung is affected, it results in diminished respiratory capacity, associated with
other symptoms; when other organs are affected, even if treated adequately, it
may leave permanent, disabling scar tissue.
WHAT
ARE THE SYMPTOMS?
The primary stage of the disease may be symptom-free, or the individual may
experience a flu-like illness. In the secondary stage, called active
disease, there might be a slight fever, night sweats, weight loss, fatigue and
various other symptoms, depending on the part of the body affected.
Tuberculosis of the lung is usually associated with a dry cough that eventually
leads to a productive cough with blood-stained sputum. There might also be
chest pain and shortness of breath. This secondary stage, if affecting the
lungs, is the contagious stage - when the bacteria can be spread to others.
HOW
DOES TUBERCULOSIS SPREAD?
The TB germ is carried on droplets in the air, and can enter the body through
the airway. A person with active pulmonary tuberculosis can spread the
disease by coughing or sneezing. The process of catching tuberculosis
involves two stages: first, a person has to become infected; second, the
infection has to progress to disease. To become infected, a person has to
come in close contact with another person having active tuberculosis. In other
words, the person has to breathe the same air in which the person with active
disease coughs or sneezes.
WHAT
ARE THE CHANCES OF BECOMING INFECTED?
A person has to come in contact with someone who has active TB disease with TB
germs present in the sputum. The likelihood of this happening also depends
on the time spent in close contact with the person with active disease.
The process of infection progresses to disease in about ten percent of those
infected, and it can happen any time during the remainder of their lives.
Although the chance of progression to disease diminishes with the passage of
time, TB can develop more easily if the immune system weakens, as happens with
malnutrition, AIDS, diabetes, cancer, or treatment with immunosuppressant drugs.
In people with both HIV and TB infection, as many as eight percent can develop
TB each year. In the United States, about one person in every 5,500 is diagnosed
as infected with TB.
IS
THERE A TREATMENT?
Yes - for either TB infection or active TB disease, antibiotic therapy can be
used. It's simpler to treat TB infection; INH taken for 6-9 months can be
completely effective. This is called preventive treatment and is an
optional program at McKinley Health Center, but is strongly recommended.
Treatment for active TB disease involves taking several anti-tuberculosis drugs
for 6-9 months, and possible initial confinement while considered infectious.
Simultaneously, you have to eat nourishing food, have adequate
rest, and follow other physician recommendations. Rarely, it may be
necessary to surgically remove a severely damaged part of an organ. After
successful treatment, you will need to undergo periodic checkups to ensure
health. It is also the only way to check for re-exposure, because once a
skin test is positive, it will always be positive.
HOW
IS TB DIAGNOSED?
Usually, the initial diagnostic/screening test for tuberculosis is the skin
test. A small amount of fluid is injected under the skin of the forearm;
the fluid contains a protein derived from the microorganism causing TB, and is
absolutely harmless to the body. The area is visually examined by a health
professional after 48-72 hours to determine the result of the test. A
positive skin test does not mean that you have active disease; rather, that you
may have been exposed to the organism referred to as TB infection at some time
in the past. If the result of the skin test is positive, a chest x-ray
must be obtained to ascertain whether there is any active disease. A
physician or a trained health professional will also review your history and may
order further tests, if necessary. If you are diagnosed with active TB,
you will be required to take medications as prescribed by the physician.
Many
individuals who grew up in countries other than the United States or Canada have
received the BCG (Bacilli Calmette-Guerin) vaccine against tuberculosis.
Studies have shown, however, that although some people are protected by this
vaccine, many are either not protected at all, or are immune for only a short
time.
If you have a positive reaction to the TB skin test and have
received BCG, the nurse will consider certain factors and advise you on what to
do next. Some of those factors may be: the extent of the reaction; whether
you come from a country with a high incidence of TB; whether you have had
contact with a person with active TB; and how many doses of BCG you have
received. BCG vaccination is not a guarantee against becoming infected
with TB, and a positive TB test is probably not due to prior vaccination with
BCG. The importance of the skin test is that it shows if you have been
exposed to tuberculosis; it helps determine if you are at risk for developing
the disease and treatment can be provided before you become sick.
WHAT
IF I DON'T TAKE THE MEDICATIONS?
As stated earlier, the primary stage of
tuberculosis infection is usually symptom-free, and ignoring the disease at this
stage will allow it to progress to the secondary stage, or allow it to flare up
later. Many times if there are symptoms, they start to disappear and you
may start feeling better after a few weeks/months of treatment. If
treatment is discontinued at this stage, or medications are not taken as
prescribed, the bacteria will have an opportunity to develop a resistance to the
drugs, and treatment will become ineffective later on. If you are
diagnosed with active TB disease, taking the medications is required, as well as
a possible initial confinement while considered infectious.
TB
TEST
In order to maintain a healthy environment for students, faculty and staff, the
University of Illinois seeks to assure that the campus is free from
tuberculosis. Because different countries have different standards of
testing and evaluating for this disease, the university requires that the
student health center test all incoming international students for TB. For
all UIUC students, the TB test is available at the Immunization and Travel
Clinic at McKinley Health Center.
Jump to A History of
Tuberculosis Chemotherapy
Jump to The Recent
TB Epidemic
Mycobacterium tuberculosis has been present in the human
population since antiquity - fragments of the spinal column from Egyptian
mummies from 2400 BCE show definite pathological signs of tubercular decay.
The term phthisis, consumption, appears first in Greek literature.
Around 460 BCE, Hippocrates identified phthisis as the most widespread disease
of the times, and noted that it was almost always fatal. Due to common phthisis
related fatalities, he wrote something no doctor would dare write today: he
warned his colleagues against visiting cases in late stages of the disease,
because their inevitable deaths might damage the reputations of the attending
physicians.
Exact pathological and anatomical descriptions of the disease began
to appear in the seventeenth century. In his Opera Medica of 1679,
Sylvius was the first to identify actual tubercles as a consistent and
characteristic change in the lungs and other areas of consumptive patients. He
also described their progression to abscesses and cavities. Manget described the
pathological features of miliary tuberculosis in 1702. The earliest references
to the infectious nature of the disease appear in seventeenth century Italian
medical literature. An edict issued by the Republic of Lucca in 1699 states
that, "henceforth, human health should no longer be endangered by objects
remaining after the death of a consumptive. The names of the deceased should be
reported to the authorities, and measures undertaken for disinfection."
In 1720, the English physician Benjamin Marten was the first to
conjecture, in his publication, A New Theory of Consumption, that TB
could be caused by "wonderfully minute living creatures", which, once
they had gained a foothold in the body, could generate the lesions and symptoms
of the disease. He stated, moreover, "It may be therefore very likely that
by an habitual lying in the same bed with a consumptive patient, constantly
eating and drinking with him, or by very frequently conversing so nearly as to
draw in part of the breath he emits from the Lungs, a consumption may be caught
by a sound person...I imagine that slightly conversing with consumptive patients
is seldom or never sufficient to catch the disease." For the early
eighteenth century, Dr. Marten's writings display a great degree of
epidemiological insight.
In contrast to this significant level of understanding about the
etiology of consumption, which was already enabling prevention and a break in
the chain of infection, those attempting to cure the disease were still groping
in the dark
The introduction of the sanatorium cure provided the first really
step against TB. Hermann Brehmer, a Silesian botany student suffering from TB,
was instructed by his doctor to seek out a healthier climate. He travelled to
the Himalayan mountains where he could pursue his botanical studies while trying
to rid himself of the disease. He returned home cured and began to study
medicine. In 1854, he presented his doctoral dissertation bearing the auspicious
title, Tuberculosis is a Curable Disease. In the same year, he built an
institution in Gorbersdorf where, in the midst of fir trees, and with good
nutrition, patients were exposed on their balconies to continuous fresh air.
This setup became the blueprint for the subsequent development of sanatoria, a
powerful weapon in the battle against an insidious opponent.
New advances then followed in rapid succession. In 1865, the French
military doctor Jean-Antoine Villemin single-handedly demonstrated that
consumption could be passed from humans to cattle and from cattle to rabbits. On
the basis of this revolutionary evidence, he postulated a specific microorganism
as the cause of the disease, finally laying to rest the centuries-old belief
that consumption arose spontaneously in each affected organism.
In 1882, Robert Koch discovered a staining technique that enabled
him to see Mycobacterium tuberculosis. What excited the world was not
so much the scientific brilliance of Koch's discovery, but the accompanying
certainty that now the fight against humanity's deadliest enemy could really
begin.
The measures available to doctors were still modest. Improving
social and sanitary conditions, and ensuring adequate nutrition were all that
could be done to strengthen the body's defenses against the TB bacillus.
Sanatoria, now to be found throughout Europe and the United States, provided a
dual function: they isolated the sick, the source of infection, from the general
population, while the enforced rest, together with a proper diet and the
well-regulated hospital life assisted the healing processes.
These efforts were reinforced by the observation of the Italian
Forlanini, that lung collapse tended to have a favorable impact on the outcome
of the disease. With the introduction of artificial pneumothorax and surgical
methods to reduce the lung volume, the depressing era of helplessness in the
face of advanced TB was over, and active therapy had begun.
A further significant advance came in 1895 when Wilhelm Konrad von
Rontgen discovered the radiation that bears his name. Now the progress and
severity of a patient's disease could be accurately followed and reviewed.
Another important development was provided by the French
bacteriologist Calmette, who, together with Guerin, used specific culture media
to lower the virulence of the bovine TB bacterium, creating the basis for the
BCG vaccine still in widespread use today. Then, in the middle of World War II,
came the final breakthrough, the greatest challenge to the bacterium that had
threatened humanity for thousands of years - chemotherapy.
In fact, the chemotherapy of infectious diseases, using sulfonamide
and penicillins, had been underway for several years, but these molecules were
ineffective against Mycobacterium tuberculosis. Since 1914, Selman A.
Waksman had been systematically screening soil bacteria and fungi, and at the
University of California in 1939 had discovered the marked inhibitory effect of
certain fungi, especially actinomycetes, on bacterial growth. In 1940, he and
his team were able to isolate an effective anti-TB antibiotic, actinomycin;
however, this proved to be too toxic for use in humans or animals
Success came in 1943. In test animals, streptomycin, purified from Streptomyces
griseus, combined maximal inhibition of M. tuberculosis with
relatively low toxicity. On November 20, 1944, the antibiotic was administered
for the first time to a critically ill TB patient. The effect was almost
immediately impressive. His advanced disease was visibly arrested, the bacteria
disappeared from his sputum, and he made a rapid recovery. The new drug had side
effects - especially on the inner ear - but the fact remained, M.
tuberculosis was no longer a bacteriological exception, it could be
assailed and beaten into retreat within the human body.
A rapid succession of anti-TB drugs appeared in the following years.
These were important because with streptomycin monotherapy, resistant mutants
began to appear with a few months, endangering the success of antibiotic
therapy. However, it was soon demonstrated that this problem could be overcome
with the combination of two or three drugs.
Following streptomycin, p-aminosalicylic acid (1949),
isoniazid (1952), pyrazinamide (1954), cycloserine (1955), ethambutol (1962) and
rifampin (rifampicin; 1963) were introduced as anti-TB agents. Aminoglycosides
such as capreomycin, viomycin, kanamycin and amikacin, and the newer quinolones
(e.g. ofloxacin and ciprofloxacin) are only used in drug resistance situations.
Combinations of a B-lactam antibiotic with a B-lactamase
inhibitor enhance treatment effectiveness, but the newer drugs, including the
macrolides, have not received much clinical testing.
Two properties of anti-TB drugs are important: antibacterial
activity, highest in
and their capacity to inhibit the development of resistance, the
most effective drugs being
With the proper four drug regimen, there should be a rapid clinical
improvement and a significant fall in the bacterial count. After a month, the
patient should be afebrile, feel well and have regained weight. Coughing and
sputum should have diminished and improvements will be visible on the X-rays.
Although bacteria will still be present in the smears, they will become more and
more difficult to culture. Improvements will be visible on the X-rays for three
to four months. If the disease was initially severe, though, the end of
treatment may not be reached for a year.
The absence of radiological improvement in the first three months
should be grounds for concern and indicate that a change in therapy is needed.
Patient compliance and the bacteria's drug sensitivity should be reevaluated.
Relapses usually occur within six months of the end of treatment, and in most
cases are due to poor patient compliance. Patient compliance must be monitored
throughout treatment; this is done at the National Tuberculosis Center through
directly
observed therapy.
When TB becomes active again in a previously treated patient, there
is a high chance that the bacteria will now be drug resistant. Any current
therapy must be suspended until multiple drugs are found to which the pathogen
is fully sensitive, and treatment can be resumed with the addition of these
drugs to the original regimen. Never add a single drug to a failing regimen. If
the microorganism is resistant to the standard drugs, then it will be necessary
to administer more toxic medications such as
The registered number of new cases of TB worldwide roughly
correlates with economic conditions: the highest incidences are seen in those
countries of Africa, Asia, and Latin America with the lowest gross national
products. WHO estimates that eight million people get TB every year, of whom 95%
live in developing countries. An estimated 3 million people die from TB every
year.
In industrialized countries, the steady drop in TB incidence began
to level off in the mid-1980s and then stagnated or even began to increase. Much
of this rise can be at least partially attributed to a high rate of immigration
from countries with a high incidence of TB. It is also difficult to perform
epidemiological surveillance and treatment in immigrant communities due to
various cultural differences.
A great influence in the rising TB trend is HIV infection. Chances
are that only one out of ten immunocompetent people infected with M.
tuberculosis will fall sick in their lifetimes, but among
those with HIV, one in ten per year will develop active TB,
while one in two or three tuberculin test positive AIDS patients will develop
active TB. In many industrialized countries this is a tragedy for the patients
involved, but it these cases make up only a small minority of TB cases. In
developing countries, the impact of HIV infection on the TB situation,
especially in the 20-35 age group, is worthy of concern.
A final factor contributing to the resurgence of TB is the emergence
of multi-drug resistance. Drug resistance in TB occurs as a result of tubercle
bacillus mutations. These mutations are not dependent upon the presence of the
drug. Exposed to a single effective anti-TB medication, the predominant bacilli,
sensitive to that drug, are killed; the few drug resistant mutants, likely to be
present if the bacterial population is large, will, multiply freely. Since it is
very unlikely that a single bacillus will spontaneously mutate to resistance to
more than one drug, giving multiple effective drugs simultaneously will inhibit
the multiplication of these resistant mutants. This is why it is absolutely
essential to treat TB patients with the recommended four drug regimen of
isoniazid, rifampin, pyrazinamide and ethambutol or streptomycin.
While wealthy industrialized countries with good public health care
systems can be expected to keep TB under control, in much of the developing
world a catastrophe awaits. It is crucially important that support be given to
research efforts devoted to developing an effective TB vaccine, shortening the
amount of time required to ascertain drug sensitivities, improving the diagnosis
of TB, and creating new, highly effective anti-TB medications. Without support
for such efforts, we run the risk of losing the battle against TB.
Tuberculosis is becoming a world-wide
problem. War, famine, homelessness, and a lack of medical care all contribute to
the increasing incidence of tuberculosis among disadvantaged persons. Since TB
is easily transmissible between persons, then the increase in TB in any segment
of the population represents a threat to all segments of the population. This
means that it is important to institute and maintain appropriate public health
measures, including screening, vaccination (where deemed of value), and
treatment. A laxity of public health measures will contribute to an increase in
cases. Failure of adequate treatment promotes the development of resistant
strains of tuberculosis.
There are two major patterns of disease
with TB:
When resistance to infection is
particularly poor, a "miliary" pattern of spread can occur in which
there are a myriad of small millet seed (1-3 mm) sized granulomas, either in
lung or in other organs.
Dissemination of tuberculosis outside of
lungs can lead to the appearance of a number of uncommon findings with
characteristic patterns:
Skeletal
Tuberculosis:
Tuberculous osteomyelitis involves mainly the thoracic and lumbar vertebrae
(known as Pott's disease) followed by knee and hip. There is extensive necrosis
and bony destruction with compressed fractures (with kyphosis) and extension to
soft tissues, including psoas "cold" abscess.
Genital
Tract Tuberculosis:
Tuberculous salpingitis and endometritis result from dissemination of
tuberculosis to the fallopian tube that leads to granulomatous salpingitis,
which can drain into the endometrial cavity and cause a granulomatous
endometritis with irregular menstrual bleeding and infertility. In the male,
tuberculosis involves prostate and epididymis most often with non-tender
induration and infertility.
Urinary
Tract Tuberculosis:
A
"sterile pyuria" with WBC's present in urine but a negative routine
bacterial culture may suggest the diagnosis of renal tuberculosis. Progressive
destruction of renal parenchyma occurs if not treated. Drainage to the ureters
can lead to inflammation with ureteral stricture.
CNS
Tuberculosis:
A meningeal pattern of spread can occur, and the cerebrospinal fluid typically
shows a high protein, low glucose, and lymphocytosis. The base of the brain is
often involved, so that various cranial nerve signs may be present. Rarely, a
solitary granuloma, or "tuberculoma", may form and manifest with
seizures.
Gastrointestinal
Tuberculosis:
This is
uncommon today because routine pasteurization of milk has eliminated
Mycobacterium bovis infections. However, M. tuberculosis organisms coughed up in
sputum may be swallowed into the GI tract. The classic lesions are
circumferential ulcerations with stricture of the small intestine. There is a
predilection for ileocecal involvement because of the abundant lymphoid tissue
and slower rate of passage of lumenal contents.
Adrenal
Tuberculosis:
Spread of tuberculosis to adrenals is usually bilateral, so that both adrenals
are markedly enlarged. Destruction of cortex leads to Addison's disease.
Scrofula:
Tuberculous lymphadenitis of the cervical nodes may produce a mass of firm,
matted nodes just under the mandible. There can be chronic draining fistulous
tracts to overlying skin. This complication may appear in children, and
Mycobacterium scrofulaceum may be cultured.
Cardiac
Tuberculosis:
The
pericardium is the usual site for tuberculous infection of heart. The result is
a granulomatous pericarditis that can be hemorrhagic. If extensive and chronic,
there can be fibrosis with calcification, leading to a constrictive pericarditis.
The following images illustrate gross
pathologic findings with tuberculosis:
1.
Ghon
complex in lung, gross.
2.
Ghon
complex in lung, closer view, gross.
3.
Cavitary
tuberculosis in lung, gross.
4.
Cavitary
tuberculosis in lung, closer view, gross.
5.
Cavitary
tuberculosis in lung, florid, gross.
6.
Miliary
tuberculosis in lung, gross.
7.
Miliary
tuberculosis in lung, closer view, gross.
Microscopically, the inflammation
produced with TB infection is granulomatous, with epithelioid macrophages and
Langhans giant cells along with lymphocytes, plasma cells, maybe a few PMN's,
fibroblasts with collagen, and characteristic caseous necrosis in the center.
The inflammatory response is mediated by a type IV hypersensitivity reaction.
This can be utilized as a basis for diagnosis by a TB skin test. An acid fast
stain (Ziehl-Neelsen or Kinyoun's acid fast stains) will show the organisms as
slender red rods. An auramine stain of the organisms as viewed under
fluorescence microscopy will be easier to screen and more organisms will be
apparent. The most common specimen screened is sputum, but the histologic stains
can also be performed on tissues or other body fluids. Culture of sputum or
tissues or other body fluids can be done to determine drug sensitivities.
1.
Granulomas
in lung, low power microscopic.
2.
Granuloma
with caseous necrosis, high power microscopic.
3.
Granuloma
with epithelioid macrophages and a Langhans giant cell, high power microscopic.
4.
Granulomatous
endometritis, high power microscopic.
5.
Ziehl-Neelsen
acid fast stain, microscopic, AFB stain.
6.
Auramine
stain, M. tuberculosis, fluorescence microscopy.
Skin testing for tuberculosis is useful
in countries where the incidence of tuberculosis is low, and the health care
system works well to detect and treat new cases. In countries where BCG
vaccination has been widely used, the TB skin test is not useful, because
persons vaccinated with BCG will have a positive skin test.
The TB skin test is based upon the type 4
hypersensitivity reaction. If a previous TB infection has occurred, then there
are sensitized lymphocytes that can react to another encounter with antigens
from TB organisms. For the TB skin test, a measured amount (the intermediate
strength of 5 tuberculin units, used in North America) of tuberculin purified
protein derivative (PPD) is injected intracutaneously to form a small wheal,
typically on the forearm. In 48 to 72 hours, a positive reaction is marked by an
area of red induration that can be measured by gentle palpation (redness from
itching and scratching doesn't count). Reactions over 10 mm in size are
considered positive in non-immunocompromised persons.
Repeated testing may increase the size of
the reaction (induration), but repeated TB skin testing will not lead to a
positive test in a person not infected by TB. Anergy, or absence of PPD
reactivity in persons infected with TB, can occur in immunocompromised persons,
or it may even occur in persons newly infected with TB, or in persons with
miliary TB.
1.
Injecting
PPD intracutaneously, gross.
2.
A
properly placed TB skin test, gross.
3.
A
positive TB skin test, gross.
Smoking is doubling the number of people dying from tuberculosis
(TB) in India, a new study warns1.
A similar cloud may be hanging over other developing countries.
About half of the 400,000 men who die from TB in India each year
do so because of smoking, the investigation found. Smoking appears to
quadruple the risk of falling ill with the disease, by helping dormant TB
bacteria blossom into a full-blown lung infection.
The result is the first convincing link between smoking and TB. It
also contrasts with the plight of smokers in the Western world, who are
more likely to die from lung cancer and heart disease. Smokers in India
also have higher rates of these diseases. "It's a surprise,"
says study member Prabhat Jha of the University of Toronto, Canada.
Researchers fear that tobacco may also exacerbate the impact of TB
in Africa, China and in other countries where the disease is rife. Women
in India and China, who rarely smoke now, might also become increasingly
vulnerable as more take up the habit.
"We're looking in the future at a real epidemic," says
Tom Glynn, director of cancer science and trends at the American Cancer
Society. Around one billion people worldwide are infected with
tuberculosis, and roughly 1.6 million die each year. It can be treated
with drugs, but these are not widely available in many developing
countries.
Even in North America and Europe, smoking might intensify TB's
impact. Although rare, the disease has returned to some places recently,
as have new drug-resistant strains. "It's a concern," says
Glynn.
Smoke screen
Previous epidemiology hinted that smoking might increase the risk
of TB. But the threat has been neglected because most studies were in the
West, where the disease is uncommon. "It just got forgotten,"
says team member and epidemiologist Richard Peto of the University of
Oxford, UK.
The group examined 43,000 men who had died in the late 1990s and a
further 35,000 still living in the southern Indian state of Tamil Nadu. TB
was far more likely to have killed smokers, they found.
Jha reckons that smoking increases people's vulnerability to
whichever disease is already widespread in a population, be it TB, cancer
or heart disease. But researchers are not sure whether quitting smoking
lowers the risks from TB as it does from cancer. |
The Global Tuberculosis Epidemic
Tuberculosis (TB) kills about two million people each year, making it one of
the world's leading infectious causes of death among young people and adults
One-third of the world's population is infected with TB. Five to 10 percent of
people who are infected with TB become sick with TB at some time during their
life]
Each year, more than 8 million people become sick with TB.[3]
Due to a combination of economic decline, the breakdown of health systems,
insufficient application of TB control measures, the spread of HIV/AIDS and the
emergence of multidrug-resistant TB (MDR-TB), TB is on the rise in many
developing and transitional economies.[4]
Between 2000 and
2020, it is estimated that:
Impact
on Women and Children
TB
is a leading cause of death among women of reproductive age and is estimated to
cause more deaths among this group than all causes of maternal mortality. [6]
Women are less likely than men to be tested and treated for TB, and
are also less likely to develop an infection. [7]
Over 250,000 children die every year of TB. Children are
particularly vulnerable to TB infection because of frequent household contact.
[8]
Regional Impact
Low- and lower-middle-income countries (those with an annual GNP per
capita of less than US$2,995) account for more than 90% of TB cases and deaths.
[9] The regions most affected by TB include:
Southeast Asia: With an estimated three million new cases of TB each
year, this is the world's hardest-hit region.
Eastern Europe: In Eastern Europe, TB deaths are increasing after
almost 40 years of steady decline.
Sub-Saharan Africa: More than 1.5 million TB cases occur in
Sub-Saharan Africa each year. This number is rising rapidly, largely due to high
prevalence of HIV.[10]
Social,
Economic, and Development Impact
Poverty, a lack of basic health services, poor nutrition, and
inadequate living conditions all contribute to the spread of TB. In turn,
illness and death from TB reinforces and deepens poverty in many communities
The average TB patient loses three to four months of work time as a
result of TB. Lost earnings can total up to 30% of annual household income.12
Some families lose 100% of their income
TB is estimated to deplete the incomes of the world's poorest
communities by a total of US$12 billion.[14]
More than 75% of TB-related disease and death occurs among people
between the ages of 15 to 54 - the most economically active segment of the
population
TB and HIV/AIDS HIV/AIDS and TB form a lethal combination, each
speeding the other's progress. HIV promotes rapid progression of primary TB
infection to active disease and is the most powerful known risk factor for
reactivation of latent TB infection to active disease
TB is a leading killer of people living with HIV/AIDS
One-third of people infected with HIV will develop TB
Prevention and Care TB infection can be prevented, treated and
contained. The World Health Organization recommends a strategy for detection and
cure called DOTS
DOTS combines five elements: political commitment, microscopy
services, drug supplies, surveillance and monitoring systems, and use of highly
efficacious regimes with direct observation of treatment
Drugs for DOTS can cost only US$10 per person for the full treatment
course (six to eight months). DOTS
is successful and has a success rate of up to 80% in the poorest countries,
prevents new infections by curing infectious patients
It has been estimated that the gap is U$300 million a year to address the TB epidemic in low and middle-income countries.
