Ailmemts & Remedies


Alternative Names: Woolsorter’s disease; Ragpicker’s disease; Cutaneous anthrax; Gastrointestinal anthrax.

Anthrax is a life-threatening infectious disease that normally affects animals, especially ruminants (such as goats, cattle, sheep, and horses). Anthrax can be transmitted to humans by contact with infected animals or their products.
Anthrax is an acute disease caused by the bacterium Bacillus anthracis. Most forms of the disease are lethal. There are effective vaccines against anthrax, and some forms of the disease respond well to antibiotic treatment.

Like many other members of the genus Bacillus, Bacillus anthracis can form dormant endospores (often referred to as “spores” for short, but not to be cnfused with fungal spores) that are able to survive in harsh conditions for decades or even centuries. Such spores can be found on all continents, even Antarctica.  When spores are inhaled, ingested, or come into contact with a skin lesion on a host they may reactivate and multiply rapidly.

Anthrax spores can be produced in vitro and used as a biological weapon. Anthrax does not spread directly from one infected animal or person to another; it is spread by spores. These spores can be transported by clothing or shoes. The dead body of an animal that died of anthrax can also be a source of anthrax spores.

In recent years, anthrax has received a great deal of attention as it has become clear that the infection can also be spread by a bioterrorist attack or by biological warfare.


There are three different types of anthrax.
1.Cutaneous anthrax ,2.Inhalational anthrax  and 3.Intestinal anthrax

1.Cutaneous anthrax – this type accounts for about 95 per cent of cases. People handling dead animals – such as abattoir workers and tanners – are at most risk. Infection occurs when the bacterium comes into direct contact with a cut or abrasion in the skin.

At first the skin itches. This is soon followed by the appearance of a small, raised itchy bump that looks like an insect bite. This skin lesion is commonly located on the head, forearms or hands.

Within one to two days the skin lesion develops into a vesicle and becomes a painless ulcer, usually about 1cm to 3cm in diameter. After two to six days the black dying central area of the ulcer that’s characteristic of cutaneous anthrax is apparent.

If left untreated, cutaneous anthrax infection can spread and cause blood poisoning, which is fatal in up to 20 per cent of cases, but with effective antibiotic treatment few deaths occur.

2.Inhalational anthrax – when inhaled, the larger spores lodge in the windpipe or throat, while smaller ones lodge further down the respiratory tract in the lungs. The anthrax bacteria produce toxins that enter the bloodstream and cause haemorrhaging and tissue decay.

Initial symptoms of inhalational anthrax, which is rare, are mild and non-specific, similar to the symptoms of a flu-like infection. These include tiredness, weakness, fever, mild non-productive cough and chest pain.

If left untreated, over the next two to six days this mild phase becomes severe, causing breathing problems, sepsis and bleeding. By the time the infection has reached this stage it’s usually fatal.

3.Intestinal anthrax
– a very rare form of food poisoning that may follow the ingestion of contaminated meat.

Initial symptoms are nausea, vomiting, loss of appetite and fever. As the infection becomes more severe, abdominal pain, vomiting of blood and severe diarrhoea occur.

Intestinal anthrax is often fatal.

Bacteria :-

Bacillus anthracis is a rod-shaped, Gram-positive, aerobic bacterium about 1 by 9 micrometers in length. It was shown to cause disease by Robert Koch in 1876. The bacterium normally rests in endospore form in the soil, and can survive for decades in this state. Herbivores are often infected whilst grazing or browsing, especially when eating rough, irritant or spiky vegetation: the vegetation has been hypothesized to cause wounds within the gastrointestinal tract permitting entry of the bacterial endo-spores into the tissues, though this has not been proven. Once ingested or placed in an open cut, the bacterium begins multiplying inside the animal or human and typically kills the host within a few days or weeks. The endo-spores germinate at the site of entry into the tissues and then spread via the circulation to the lymphatics, where the bacteria multiply.


Occupational exposure to infected animals or their products (such as skin, wool, and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common. Anthrax in livestock grazing on open range where they mix with wild animals still occasionally occurs in the United States and elsewhere. Many workers who deal with wool and animal hides are routinely exposed to low levels of anthrax spores but most exposures are not sufficient to develop anthrax infections. It is presumed that the body’s natural defenses can destroy low levels of exposure. These people usually contract cutaneous anthrax if they catch anything. Throughout history, the most dangerous form of inhalational anthrax was called Woolsorters’ disease because it was an occupational hazard for people who sorted wool. Today this form of infection is extremely rare, as almost no infected animals remain. The last fatal case of natural inhalational anthrax in the United States occurred in California in 1976, when a home weaver died after working with infected wool imported from Pakistan. The autopsy was done at UCLA hospital. To minimize the chance of spreading the disease, the deceased was transported to UCLA in a sealed plastic body bag within a sealed metal container.


Respiratory infection in humans initially presents with cold or flu-like symptoms for several days, followed by severe (and often fatal) respiratory collapse. Historical mortality was 92%, but, when treated early (seen in the 2001 anthrax attacks), observed mortality was 45%. Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed. Illness progressing to the fulminant phase has a 97% mortality regardless of treatment.


Gastrointestinal infection in humans is most often caused by eating anthrax-infected meat and is characterized by serious gastrointestinal difficulty, vomiting of blood, severe diarrhea, acute inflammation of the intestinal tract, and loss of appetite. Some lesions have been found in the intestines and in the mouth and throat. After the bacterium invades the bowel system, it spreads through the bloodstream throughout the body, making even more toxins on the way. Gastrointestinal infections can be treated but usually result in fatality rates of 25% to 60%, depending upon how soon treatment commences.  This form of anthrax is the rarest form. In the United States, there is only one official case reported in 1942 by the CDC.

Cutaneous :

Anthrax skin lesionCutaneous (on the skin) anthrax infection in humans shows up as a boil-like skin lesion that eventually forms an ulcer with a black center (eschar). The black eschar often shows up as a large, painless necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between 2 and 5 days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain.

Mode of infection :-
Inhalational anthrax, mediastinal wideningAnthrax can enter the human body through the intestines (ingestion), lungs (inhalation), or skin (cutaneous) and causes distinct clinical symptoms based on its site of entry. In general, an infected human will be quarantined. However, anthrax does not usually spread from an infected human to a noninfected human. But, if the disease is fatal to the person’s body, its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent further contamination. Inhalational anthrax, if left untreated until obvious symptoms occur, may be fatal.

Anthrax can be contracted in laboratory accidents or by handling infected animals or their wool or hides. It has also been used in biological warfare agents and by terrorists to intentionally infect as exemplified by the 2001 anthrax attacks.

Other than Gram Stain of specimens, there are no specific direct identification techniques for identification of Bacillus species in clinical material. These organisms are Gram-positive but with age can be Gram-variable to Gram-negative. A specific feature of Bacillus species that makes it unique from other aerobic microorganisms is its ability to produce spores. Although spores are not always evident on a Gram stain of this organism, the presence of spores confirms that the organism is of the genus Bacillus.

All Bacillus species grow well on 5% Sheep blood agar and other routine culture media. PLET (polymyxin-lysozyme-EDTA-thallous acetate) can be used to isolate B.anthracis from contaminated specimens, and bicarbonate agar is used as an identification method to induce capsule formation.

Bacillus sp. will usually grow within 24 hours of incubation at 35 degrees C, in ambient air (room temperature) or in 5% CO2. If bicarbonate agar is used for identification then the media must be incubated in 5% CO2.

B.anthracis appears as medium-large, gray, flat, irregular with swirling projections, often referred to as “medusa head” appearance, and is non-hemolytic on 5% sheep blood agar. It is non-motile, is susceptible to penicillin and produces a wide zone of lecithinase on egg yolk agar. Confirmatory testing to identify B.anthracis includes gamma bacteriophage testing, indirect hemagglutination and enzyme linked immunosorbent assay to detect antibodies.

Anthrax cannot be spread directly from person to person, but a patient’s clothing and body may be contaminated with anthrax spores. Effective decontamination of people can be accomplished by a thorough wash-down with antimicrobial effective soap and water. Waste water should be treated with bleach or other anti-microbial agent. Effective decontamination of articles can be accomplished by boiling contaminated articles in water for 30 minutes or longer. Chlorine bleach is ineffective in destroying spores and vegetative cells on surfaces, though formaldehyde is effective. Burning clothing is very effective in destroying spores. After decontamination, there is no need to immunize, treat or isolate contacts of persons ill with anthrax unless they were also exposed to the same source of infection. Early antibiotic treatment of anthrax is essential—delay significantly lessens chances for survival. Treatment for anthrax infection and other bacterial infections includes large doses of intravenous and oral antibiotics, such as fluoroquinolones, like ciprofloxacin (cipro), doxycycline, erythromycin, vancomycin or penicillin. In possible cases of inhalation anthrax, early antibiotic prophylaxis treatment is crucial to prevent possible death. In May 2009, Human Genome Sciences submitted a Biologic License Application (BLA, permission to market) for its new drug, raxibacumab (brand name ABthrax) intended for emergency treatment of inhaled anthrax.[28] If death occurs from anthrax the body should be isolated to prevent possible spread of anthrax germs. Burial does not kill anthrax spores.

If a person is suspected as having died from anthrax, every precaution should be taken to avoid skin contact with the potentially contaminated body and fluids exuded through natural body openings. The body should be put in strict quarantine. A blood sample taken in a sealed container and analyzed in an approved laboratory should be used to ascertain if anthrax is the cause of death. Microscopic visualization of the encapsulated bacilli, usually in very large numbers, in a blood smear stained with polychrome methylene blue (McFadyean stain) is fully diagnostic, though culture of the organism is still the gold standard for diagnosis. Full isolation of the body is important to prevent possible contamination of others. Protective, impermeable clothing and equipment such as rubber gloves, rubber apron, and rubber boots with no perforations should be used when handling the body. No skin, especially if it has any wounds or scratches, should be exposed. Disposable personal protective equipment is preferable, but if not available, decontamination can be achieved by autoclaving. Disposable personal protective equipment and filters should be autoclaved, and/or burned and buried. Bacillus anthracis bacillii range from 0.5–5.0 ?m in size. Anyone working with anthrax in a suspected or confirmed victim should wear respiratory equipment capable of filtering this size of particle or smaller. The US National Institute for Occupational Safety and Health (NIOSH) and Mine Safety and Health Administration (MSHA) approved high efficiency-respirator, such as a half-face disposable respirator with a high-efficiency particulate air (HEPA) filter, is recommended.[29] All possibly contaminated bedding or clothing should be isolated in double plastic bags and treated as possible bio-hazard waste. The victim should be sealed in an airtight body bag. Dead victims that are opened and not burned provide an ideal source of anthrax spores. Cremating victims is the preferred way of handling body disposal. No embalming or autopsy should be attempted without a fully equipped biohazard laboratory and trained and knowledgeable personnel.

Delays of only a few days may make the disease untreatable and treatment should be started even without symptoms if possible contamination or exposure is suspected. Animals with anthrax often just die without any apparent symptoms. Initial symptoms may resemble a common cold—sore throat, mild fever, muscle aches and malaise. After a few days, the symptoms may progress to severe breathing problems and shock and ultimately death. Death can occur from about two days to a month after exposure with deaths apparently peaking at about 8 days after exposure.[30] Antibiotic-resistant strains of anthrax are known.

In recent years there have been many attempts to develop new drugs against anthrax, but existing drugs are effective if treatment is started soon enough.

Early detection of sources of anthrax infection can allow preventive measures to be taken. In response to the anthrax attacks of October 2001 the United States Postal Service (USPS) installed BioDetection Systems (BDS) in their large scale mail cancellation facilities. BDS response plans were formulated by the USPS in conjunction with local responders including fire, police, hospitals and public health. Employees of these facilities have been educated about anthrax, response actions and prophylactic medication. Because of the time delay inherent in getting final verification that anthrax has been used, prophylactic antibiotic treatment of possibly exposed personnel must be started as soon as possible.

When treated with antibiotics, cutaneous anthrax is likely to get better. However, up to 20% of people who do not get treatment may die due to anthrax-related blood infections.

People with second-stage inhalation anthrax have a poor outlook, even with antibiotic therapy. Up to 90% of cases in the second stage are fatal.

Gastrointestinal anthrax infection can spread to the bloodstream, and may result in death.

Possible Complications:

Cutaneous anthrax:
•Spread of infection into the bloodstream

Inhalational anthrax:

•Hemorrhagic meningitis
•Swelling of lymph nodes in the chest (mediastinal adenopathy)
•Fluid buildup in the chest (pleural effusion)

Gastrointestinal anthrax
•Severe bleeding (hemorrhage)

There are two main ways to prevent anthrax.

For people who have been exposed to anthrax (but have no symptoms of the disease), doctors may prescribe preventive antibiotics, such as ciprofloxacin, penicillin, or doxycycline, depending on the strain of anthrax.

An anthrax vaccine is available to certain military personnel, but not to the general public. It is given in a series of six doses over 18 months. There is no known way to spread cutaneous anthrax from person to person. People who live with someone who has cutaneous anthrax do not need antibiotics unless they have also been exposed to the same source of anthrax.

An anthrax vaccine licensed by the U.S. Food and Drug Administration (FDA) and produced from one non-virulent strain of the anthrax bacterium, is manufactured by BioPort Corporation, subsidiary of Emergent BioSolutions. The trade name is BioThrax, although it is commonly called Anthrax Vaccine Adsorbed (AVA). It was formerly administered in a six-dose primary series at 0, 2, 4 weeks and 6, 12, 18 months, with annual boosters to maintain immunity. On December 11, 2008, the FDA approved the removal of the 2-week dose, resulting in the currently recommended five-dose series.

Unlike NATO countries, the Soviets developed and used a live spore anthrax vaccine, known as the STI vaccine, produced in Tbilisi, Georgia. Its serious side-effects restrict use to healthy adults.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

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Ailmemts & Remedies

Tuberculosis (TB)

Tuberculosis (TB) is a bacterial infection caused by a germ called Mycobacterium tuberculosis. The bacteria usually attack the lungs, but they can also damage other parts of the body. TB spreads through the air when a person with TB of the lungs or throat coughs, sneezes or talks. If you have been exposed, you should go to your doctor for tests. You are more likely to get TB if you have a weak immune system.

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Tuberculosis (abbreviated as TB for tubercle bacillus or Tuberculosis) is a common and often deadly infectious disease caused by mycobacteria, mainly Mycobacterium tuberculosis. Tuberculosis usually attacks the lungs (as pulmonary TB) but can also affect the central nervous system, the lymphatic system, the circulatory system, the genitourinary system, the gastrointestinal system, bones, joints, and even the skin. Other mycobacteria such as Mycobacterium bovis, Mycobacterium africanum, Mycobacterium canetti, and Mycobacterium microti also cause tuberculosis, but these species are less common

Other names
In the past, tuberculosis has been 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. 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. TB is also called Koch’s disease after the scientist Robert Koch.

Click to see:->Tuberculosis classification
The typical symptoms of tuberculosis are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss. Infection of other organs causes a wide range of symptoms. The diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids. Tuberculosis treatment is difficult and requires long courses of multiple antibiotics. Contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensively) multi-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin (BCG vaccine).

Symptoms of TB in the lungs may include:

*A bad cough that lasts 3 weeks or longer
*Weight loss
*Coughing up blood or mucus
*Weakness or fatigue
*Fever and chills
*Night sweats

If not treated properly, TB can be deadly. You can usually cure active TB by taking several medicines for a long period of time. People with latent TB can take medicine so that they do not develop active TB.

Tuberculosis is spread through the air, when people who have the disease cough, sneeze, or spit. One third of the world’s current population have been infected with M. tuberculosis, and new infections occur at a rate of one per second. However, most of these cases will not develop the full-blown disease; asymptomatic, latent infection is most common. About one in ten of these latent infections will eventually progress to active disease, which, if left untreated, kills more than half of its victims. In 2004, mortality and morbidity statistics included 14.6 million chronic active cases, 8.9 million new cases, and 1.6 million deaths, mostly in developing countries. 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 AIDS. The distribution of tuberculosis is not uniform across the globe with about 80% of the population in many Asian and African countries testing positive in tuberculin tests, while only 5-10% of the US population testing positive.It is estimated that the US has 25,000 new cases of tuberculosis each year, 40% of which occur in immigrants from countries where tuberculosis is endemic.

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.

In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB. This occurs more commonly 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.


It is a Bacterial Infection:

Bacterial species
Click to see
->: Mycobacterium tuberculosis
click & see
Scanning electron micrograph of Mycobacterium tuberculosisThe primary cause of TB, Mycobacterium tuberculosis, 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.[8] (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 Gram-positive or does not retain dye due to the high lipid & mycolic acid content of its cell wall.[9] 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
How does a person get TB?
A person can become infected with tuberculosis bacteria when he or she inhales minute particles of infected sputum from the air. The bacteria get into the air when someone who has a tuberculosis lung infection coughs, sneezes, shouts, or spits (which is common in some cultures). People who are nearby can then possibly breathe the bacteria into their lungs. You don’t get TB by just touching the clothes or shaking the hands of someone who is infected. Tuberculosis is spread (transmitted) primarily from person to person by breathing infected air during close contact.

There is a form of atypical tuberculosis, however, that is transmitted by drinking unpasteurized milk. Related bacteria, called Mycobacterium bovis, cause this form of TB. Previously, this type of bacteria was a major cause of TB in children, but it rarely causes TB now since most milk is pasteurized (undergoes a heating process that kills the bacteria).

How common is TB, and who gets it?
Over 8 million new cases of TB occur each year worldwide. In the United States, it is estimated that 10-15 million people are infected with the TB bacteria and 22,000 new cases of TB occur each year.

Anyone can get TB, but certain people are at higher risk, including
*people who live with individuals who have an active TB infection,

*poor or homeless people,

*foreign-born people from countries that have a high prevalence of TB,

*nursing home residents and prison inmates,

*alcoholics and intravenous drug users,

*people with diabetes, certain cancers, and HIV infection (the AIDS virus), and

*health-care workers.
There is no strong evidence for a genetically determined (inherited) susceptibility for TB.


Tuberculosis is diagnosed definitively by identifying the causative organism (Mycobacterium tuberculosis) in a clinical sample (for example, sputum or pus). When this is not possible, a probable diagnosis may be made using imaging (X-rays or scans) and/or a tuberculin skin & see
TB can be diagnosed in several different ways, including chest x-rays, analysis of sputum, and skin tests. Sometimes, the chest x-rays can reveal evidence of active tuberculosis pneumonia. Other times, the x-rays may show scarring (fibrosis) or hardening (calcification) in the lungs, suggesting that the TB is contained and inactive. Examination of the sputum on a slide (smear) under the microscope can show the presence of the tuberculosis-like bacteria. Bacteria of the mycobacterium family, including atypical mycobacteria, stain positive with special dyes and are referred to as acid-fast bacteria (AFB). A sample of the sputum also is usually taken and grown (cultured) in special incubators so that the tuberculosis bacteria can subsequently be identified as tuberculosis or atypical tuberculosis.

Several types of skin tests are used to screen for TB infection. These so-called tuberculin skin tests include the Tine test and the Mantoux test, also known as the PPD (purified protein derivative) test. In each of these tests, a small amount of purified extract from dead tuberculosis bacteria is injected under the skin. If a person is not infected with TB, then no reaction will occur at the site of the injection (a negative skin test). If a person is infected with tuberculosis, however, a raised and reddened area will occur around the site of the test injection. This reaction, a positive skin test, occurs about 48 to 72 hours after the injection.

If the infection with tuberculosis has occurred recently, however, the skin test can be falsely negative. The reason for a false negative test with a recent infection is that it usually takes two to 10 weeks after the time of infection with tuberculosis before the skin test becomes positive. The skin test can also be falsely negative if a person’s immune system is weakened or deficient due to another illness such as AIDS or cancer, or while taking medications that can suppress the immune response, such as cortisone or anticancer drugs.

Remember, however, that the TB skin test cannot determine whether the disease is active or not. This determination requires the chest x-rays and/or sputum analysis (smear and culture) in the laboratory. The organism can take up to six weeks to grow in culture in the microbiology lab. A special test to diagnose TB called the PCR (polymerase chain reaction) detects the genetic material of the bacteria. This test is extremely sensitive (it detects minute amounts of the bacteria) and specific (it detects only the TB bacteria). One can usually get results from the PCR test within a few days.

Progression from TB infection to TB disease occurs when the TB bacilli overcome the immune system defenses and begin to multiply. In primary TB disease—1–5% of cases—this occurs soon after infection. However, in the majority of cases, a latent infection occurs that has no obvious symptoms. These dormant bacilli can produce tuberculosis in 2–23% of these latent cases, often many years after infection. 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.

Patients with diabetes mellitus are at increased risk of contracting tuberculosis, and they have a poorer response to treatment, possibly due to poorer drug absorption

Other conditions that increase risk include IV drug abuse; recent TB infection or a history of inadequately treated TB; chest X-ray suggestive of previous TB, showing fibrotic lesions and nodules; 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; vitamin D deficiency;and low body weight.

Twin studies in the 1940s showed that susceptibility to TB was heritable. If one of a pair of twins got TB, then and the other was more likely to get TB if he was identical than if he was not. Since then, specific gene polymorphisms in IL12B have been linked to tuberculosis susceptibility.

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.

A person with a positive skin test, a normal chest x-ray, and no symptoms most likely has only a few TB germs in an inactive state and is not contagious. Nevertheless, treatment with an antibiotic may be recommended for this person to prevent the TB from turning into an active infection. The antibiotic used for this purpose is called isoniazid (INH). If taken for six to 12 months, it will prevent the TB from becoming active in the future. In fact, if a person with a positive skin test does not take INH, there is a 5%-10% lifelong risk that the TB will become active.

Taking isoniazid can be inadvisable (contraindicated) during pregnancy or for those suffering from alcoholism or liver disease. Also, isoniazid can have side effects. The side effects occur infrequently, but a rash can develop, and the patient can feel tired or irritable. Liver damage from isoniazid is a rare occurrence and typically reverses once the drug is stopped. Very rarely, however, especially in older people, the liver damage (INH hepatitis) can even be fatal. It is important therefore, for the doctor to monitor a patient’s liver by periodically ordering blood tests called “liver function tests” during the course of INH therapy. Another side effect of INH is a decreased sensation in the extremities referred to as a peripheral neuropathy. This can be avoided by taking vitamin B6 (pyridoxine), and this is often prescribed along with INH.

A person with a positive skin test along with an abnormal chest x-ray and sputum evidencing TB bacteria has active TB and is contagious. As already mentioned, active TB usually is accompanied by symptoms, such as a cough, fever, weight loss, and fatigue.

Active TB is treated with a combination of medications along with isoniazid. Rifampin (Rifadin), ethambutol (Myambutol), and pyrazinamide are the drugs commonly used to treat active TB in conjunction with isoniazid (INH). Four drugs are often taken for the first two months of therapy to help kill any potentially resistant strains of bacteria. Then the number is usually reduced to two drugs for the remainder of the treatment based on drug sensitivity testing that is usually available by this time in the course. Streptomycin, a drug that is given by injection, may be used as well, particularly when the disease is extensive and/or the patients do not take their oral medications reliably (termed “poor compliance”). Treatment usually lasts for many months and sometimes for years. Successful treatment of TB is dependent largely on the compliance of the patient. Indeed, the failure of a patient to take the medications is the most important cause of failure to cure the TB infection. In some locations, the health department demands direct monitoring of patient compliance with therapy.

Surgery on the lungs may be indicated to help cure TB when medication has failed, but in this day and age, surgery for TB is unusual. Treatment with appropriate antibiotics will usually cure the TB. Without treatment, however, tuberculosis can be a lethal infection. Therefore, early diagnosis is important. Those individuals who have been exposed to a person with TB, or suspect that they have been, should be examined by a doctor for signs of TB and screened with a TB skin test.

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. 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. People with 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.

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. Drug-resistant TB is a public health issue in many developing countries, as treatment is longer and requires more expensive drugs. Multi-drug 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.

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”.  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. 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.

Click to learn more about:-> Tuberculosis treatment

What is drug-resistant TB?
Drug-resistant TB (TB that does not respond to drug treatment) has become a very serious problem in recent years in certain populations. For example, INH-resistant TB is seen among patients from Southeast Asia. The presence of INH-like substances in the cough syrups in that part of the world may play a role in causing the INH resistance. Drug-resistant cases are also often seen in prison populations. However, the major reason for the development of resistance is poorly managed TB care. This can result from poor patient compliance, inappropriate dosing or prescribing of medication, poorly formulated medications, and/or an inadequate supply of medication. Multidrug-resistant tuberculosis (MDR-TB) refers to organisms that are resistant to at least two of the first-line drugs, INH and Rifampin. More recently, extensively (extremely) drug resistant tuberculosis (XDR-TB) has emerged. These bacteria are also resistant to three or more of the second-line treatment drugs.

XDR-TB is seen throughout the world but is most frequently seen in the countries of the former Soviet Union and Asia.

Preventing XDR-TB from spreading is essential. The World Health Organization (WHO) recommends improving basic TB care to prevent emergence of resistance and the development of proper laboratories for detection of resistant cases. When drug-resistant cases are found, prompt, appropriate treatment is required. This will prevent further transmission. Collaboration of HIV and TB care will also help limit the spread of tuberculosis, both sensitive and resistant strains.
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 levels of other species of mycobacteria are high, exposure to nontuberculous mycobacteria gives some protection against TB.

The World Health Organization (W.H.O.) 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. Since humans are the only host of Mycobacterium tuberculosis, eradication would be possible: a goal that would be helped greatly by an effective vaccine.

Many countries use Bacillus Calmette-Guérin (BCG) vaccine as part of their TB control programs, especially for infants. According to the W.H.O., this is the most often used vaccine worldwide, with 85% of infants in 172 countries immunized in 1993.  This was the first vaccine for TB and developed at the Pasteur Institute in France between 1905 and 1921.  However, mass vaccination with BCG did not start until after World War II. 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%.

In South Africa, the country with the highest prevalence of TB, BCG is given to all children under age three. However, BCG is less effective 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:

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.
BCG provides some protection against severe forms of pediatric TB, but has been shown to be unreliable against adult pulmonary TB, which accounts for most of the disease burden worldwide. Currently, there are more cases of TB on the planet than at any other time in history and most agree there is an urgent need for a newer, more effective vaccine that would prevent all forms of TB—including drug resistant strains—in all age groups and among people with HIV.

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). 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. A very promising TB vaccine, MVA85A, is currently in phase II trials in South Africa by a group led by Oxford University, and is based on a genetically modified vaccinia virus. Many other strategies are also being used to develop novel vaccines. In order to encourage further discovery, researchers and policymakers are promoting new economic models of vaccine development including prizes, tax incentives and advance market commitments.

The Bill and Melinda Gates Foundation has been a strong supporter of new TB vaccine development. Most recently, they announced a $200 million grant to the Aeras Global TB Vaccine Foundation for clinical trials on up to six different TB vaccine candidates currently in the pipeline.

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Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.