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Tuberculosis (TB)


Tuberculosis or TB (short for Tubercle Bacillus) is a common and often deadly infectious disease caused by mycobacteria, usually Mycobacterium tuberculosis in humans.[1] Tuberculosis usually attacks the lungs but can also affect other parts of the body. It is spread through the air, when people who have the disease cough, sneeze, or spit. Most infections in humans result in an asymptomatic, latent infection, and about one in ten latent infections eventually progresses to active disease, which, if left untreated, kills more than 50% of its victims.


Watch closely…


TB - Infected


The classic symptoms are a chronic cough with blood-tinged sputumfevernight sweats, and weight loss. Infection of other organs causes a wide range of symptoms.Diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids.Treatment is difficult and requires long courses of multiple antibiotics. Contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensivelymulti-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin vaccine.

A third of the world’s population are thought to be infected with M. tuberculosis,[2] and new infections occur at a rate of about one per second.[3] The proportion of people who become sick with tuberculosis each year is stable or falling worldwide but, because of population growth, the absolute number of new cases is still increasing.[3] In 2007 there were an estimated 13.7 million chronic active cases, 9.3 million new cases, and 1.8 million deaths, mostly in developing countries.[4] In addition, more people in the developed world are contracting tuberculosis because their immune systems are compromised by immunosuppressive drugssubstance abuse, or AIDS. The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries test positive in tuberculin tests, while only 5-10% of the US population test positive.[1]



The current clinical classification system for tuberculosis (TB) is based on the pathogenesis of the disease.[citation needed]

Classification System for TB
Class Type Description
0 No TB exposure
Not infected
No history of exposure
Negative reaction to tuberculin skin test
1 TB exposure
No evidence of infection
History of exposure
Negative reaction to tuberculin skin test
2 TB infection
No disease
Positive reaction to tuberculin skin test
Negative bacteriologic studies (if done)
No clinical, bacteriologic, or radiographic evidence of TB
3 TB, clinically active M. tuberculosis cultured (if done)
Clinical, bacteriologic, or radiographic evidence of current disease
4 TB
Not clinically active
History of episode(s) of TB
Abnormal but stable radiographic findings
Positive reaction to the tuberculin skin test
Negative bacteriologic studies (if done)
No clinical or radiographic evidence of current disease
5 TB suspect Diagnosis pending
TB disease should be ruled in or out within 3 months

Signs and symptoms

File:Tuberculosis symptoms.svg

TB-Signs & Symptoms

When the disease becomes active, 75% of the cases are pulmonary TB, that is, TB in the lungs. Symptoms include chest paincoughing up blood, and a productive, prolonged cough for more than three weeks. Systemic symptoms include feverchillsnight sweatsappetite lossweight losspallor, and often a tendency to fatigue very easily.[3]

In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted extrapulmonary tuberculosis.[7] This occurs more commonly inimmunosuppressed persons and young children. Extrapulmonary infection sites include the pleura in tuberculosis pleurisy, 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. Extrapulmonary TB may co-exist with pulmonary TB as well.[8]



The primary cause of TB, Mycobacterium tuberculosis, is a small aerobic non-motile bacillus. High lipid content of this pathogen accounts for many of its unique clinical characteristics.[9] It divides every 16 to 20 hours, an extremely slow rate compared with other bacteria, which usually divide in less than an hour.[10] (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 aGram-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.[11] MTB can withstand weak disinfectants and survive in a dry state for weeks. In nature, the bacterium can grow only within the cells of a host organism, but M. tuberculosis can be cultured in vitro.[12]



Using histological stains on expectorate samples from phlegm (also called sputum), scientists can identify MTB under a regular microscope. Since MTB retains certain stains after being treated with acidic solution, it is classified as an acid-fast bacillus (AFB).[1][11] The most common acid-fast staining technique, the Ziehl-Neelsen stain, dyes AFBs a bright red that stands out clearly against a blue background. Other ways to visualize AFBs include an auramine-rhodamine stain and fluorescent microscopy.

The M. tuberculosis complex includes four other TB-causing mycobacteriaM. bovisM. africanumM. canetti and M. microti.[13] M. africanum is not widespread, but in parts of Africa it is a significant cause of tuberculosis.[14][15] M. bovis was once a common cause of tuberculosis, but the introduction of pasteurized milk has largely eliminated this as a public health problem in developed countries.[1][16] M. canetti is rare and seems to be limited to Africa, although a few cases have been seen in African emigrants.[17] M. microti is mostly seen in immunodeficient people, although it is possible that the prevalence of this pathogen has been underestimated.[18]

Other known pathogenic mycobacteria include Mycobacterium lepraeMycobacterium avium and M. kansasii. The last two are part of the nontuberculous mycobacteria (NTM) group. Nontuberculous mycobacteria cause neither TB nor leprosy, but they do cause pulmonary diseases resembling TB.[19]



Treatment for TB uses antibiotics to kill the bacteria. Effective TB treatment is difficult, due to the unusual structure and chemical composition of the mycobacterial cell wall, which makes many antibiotics ineffective and hinders the entry of drugs.[71][72][73][74] 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 24 months) to entirely eliminate mycobacteria from the body.[8] 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.[75] People with latent infections are treated to prevent them from progressing to active TB disease later in life.

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.[75] Drug-resistant TB is a public health issue in many developing countries, as treatment is longer and requires more expensive drugs. Multi-drug-resistant tuberculosis (MDR-TB) is defined as resistance to the two most effective first-line TB drugs: rifampicin andisoniazidExtensively drug-resistant TB (XDR-TB) is also resistant to three or more of the six classes of second-line drugs.[76] The DOTS (Directly Observed Treatment Short-course) strategy of tuberculosis treatment recommended by WHO was based on clinical trials done in the 1970s by Tuberculosis Research Centre, Chennai, India. The country in which a person with TB lives can determine what treatment they receive. This is because multidrug-resistant tuberculosis is resistant to most first-line medications, the use of alternative treatments, often referred to as “second-line” antituberculosis medications, is necessary to cure the patient. However, the price of these medications is high; thus poor people in the developing world have no or limited access to these treatments.[77]



The Mycobacterium Tuberculosis Structural Genomics Consortium is a global consortium of scientists conducting research regarding the diagnosis and treatment of tuberculosis. They are attempting to determine the 3-dimensional structures of proteins from M. Tuberculosis.[citation needed]


Infection of other animals

Tuberculosis can be carried by mammals; domesticated species, such as cats and dogs, are generally free of tuberculosis, but wild animals may be carriers.

Mycobacterium bovis causes TB in cattle. An effort to eradicate bovine tuberculosis from the cattle and deer herds of New Zealand is underway. It has been found that herd infection is more likely in areas where infected natural reservoir such as Australian brush-tailed possums come into contact with domestic livestock at farm/bush borders.[145] Controlling the vectors through possum eradication and monitoring the level of disease in livestock herds through regular surveillance are seen as a “two-pronged” approach to ridding New Zealand of the disease.

In the Republic of Ireland and the United Kingdom, badgers have been identified as one vector species for the transmission of bovine tuberculosis. As a result, governments have come under pressure from some quarters, primarily dairy farmers, to mount an active campaign of eradication of badgers in certain areas with the purpose of reducing the incidence of bovine TB. The effectiveness of culling on the incidence of TB in cattle is a contentious issue, with proponents and opponents citing their own studies to support their position.[146][147][148] For instance, a study by an Independent Study Group on badger culling reported on 18 June 2007 that it was unlikely to be effective and would only make a “modest difference” to the spread of TB and that “badger culling cannot meaningfully contribute to the future control of cattle TB”; in contrast, another report concluded that this policy would have a significant impact.[149] On 4 July 2008, the UK government decided against a proposed random culling policy.[150]



  1. a b c d e f g h i j k l m n o p q r Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 516–522. ISBN 978-1-4160-2973-1.
  2. ^ Jasmer RM, Nahid P, Hopewell PC (December 2002). “Clinical practice. Latent tuberculosis infection”N. Engl. J. Med. 347 (23): 1860–6. doi:10.1056/NEJMcp021045PMID 12466511.
  3. a b c d e “Tuberculosis”. World Health Organization. 2007. Retrieved 12 November 2009. Fact sheet No 104.
  4. a b c World Health Organization (2009). “Epidemiology”Global tuberculosis control: epidemiology, strategy, financing. pp. 6–33. ISBN 978 92 4 156380 2. Retrieved 12 November 2009.
  5. ^ Tuberculosis Symptoms From eMedicineHealth. Author: George Schiffman, MD, FCCP. Last Editorial Review: 1/15/2009
  6. ^ Additional symptoms for primary/early pulmonary infection: –> Diseases » Tuberculosis » Symptoms Retrieved on 1 June 2009
  7. ^ Extrapulmonary Tuberculosis: An Overview MARJORIE P. GOLDEN, M.D., Yale University School of Medicine and Hospital of Saint Raphael, New Haven, Connecticut. HOLENARASIPUR R. VIKRAM, M.D., Mayo Clinic, Scottsdale, Arizona.
  8. a b c d e f Centers for Disease Control and Prevention (CDC), Division of Tuberculosis Elimination. Core Curriculum on Tuberculosis: What the Clinician Should Know. 4th edition (2000). Updated August 2003.
  9. ^ Southwick, Frederick (10 December 2007). “Chapter 4: Pulmonary Infections”Infectious Diseases: A Clinical Short Course, 2nd ed.. McGraw-Hill Medical Publishing Division. p. 104. ISBN 0071477225.
  10. ^ Cox R (2004). “Quantitative relationships for specific growth rates and macromolecular compositions of Mycobacterium tuberculosisStreptomyces coelicolor A3(2) and Escherichia coli B/r: an integrative theoretical approach”Microbiology150 (Pt 5): 1413–26. doi:10.1099/mic.0.26560-0PMID 15133103.

January 27, 2010 - Posted by | Blood


  1. what is the best combination to fight TB not using Synthetic Drugs but Supplements?

    Comment by Mark Sibulo | November 25, 2010 | Reply

    • The best combination of nutritional supplement for Tuberculosis are the following:
      Essentials 3x /day preferably after meal.
      CoQuinone & Biomega (twice a day preferably after meal).
      Continue this recommendation for 6 to 8 weeks.

      Thanks and God bless!

      Comment by Engr. Ardy Motos | November 25, 2010 | Reply

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