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.

 

Brief History of Tuberculosis

 


Jump to A History of Tuberculosis Chemotherapy

Jump to Chemotherapy Today

Jump to The Recent TB Epidemic

A History of Tuberculosis Treatment

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.

A History of Tuberculosis 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.

Chemotherapy Today

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 Recent TB Epidemic

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.


 

Pathology of Tuberculosis


 General features

 

 Mycobacterium tuberculosis is the organism that is the causative agent for tuberculosis (TB). There are other "atypical" mycobacteria such as M. kansasii that may produced a similar clincal and pathologic appearance of disease. M. avium-intracellulare (MAI) seen in immunocompromised hosts (particularly in persons with AIDS) is not primarily a pulmonary infection in terms of its organ distribution (mostly in organs of the mononuclear phagocyte system).

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.

Patterns of Infection

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.

Microscopic Findings

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.

Tuberculin Skin Testing

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.


  

HELEN PEARSON

Around 1 billion people catch TB each year.

WHO

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.