The pathophysiology of tuberculosis can be discussed from few aspects which are, latent tuberculosis and reactivation of tuberculosis; pulmonary and extrapulmonary tuberculosis ;as well as from the aspect of immunopathology.
Initially the bacterial mycobacterial tuberculosis bacilli are inhaled via air into the lungs. In the lungs they will trigger immune response. T-lymphocytes will be released into the lungs. There are two types of T- lymphocytes which are T helper type 1 and T helper type 2[1]. There are some CD4 co -receptors on the membrane of T cells, assisting the T -cell receptors by amplifying the signal generated by T -cells receptors this is done by recruiting a tyrosine kinase KK enzyme. When T cells are activated they will produce some chemicals known as Tumour Necrosis Factor a and INF gamma cytokines, these enzymes will then activate the macrophages which will then engulf the bacteria. Complement system also plays a role in phargocytosis of bacterial ,protein C -3 are released and bind to the cell wall of bacterial, enhancing the recognition and phargocytosis of mycobacterial by macrophages[2]. Macrophages will produce proteolytic enzymes and cytokines in attempt to degrade the bacteria. The engulfed bacteria will be stopped from spreading and reproducing thus inhibiting their actions. T -lymphocytes also play a role in degrading the immature macrophages since these macrophages are unable to inhibit the bacterial but will promote their growth indirectly. This is known as latent tuberculosis infection since the bacterial are successfully been wrapped by macrophages as granuloma and stop reproducing, there is no infection and symptoms of tuberculosis ,the bacterial remain dormant. Sometimes the granuloma can even be calcified making the scar harder. Actually the bacterial can inhibit the fusion of macrophage lysosomes to phargosomes, so that they are not degraded by macrophage. Besides that, lipoarabinomanna of the bacterial also can induce immunosuppressive cytokines which in return will block the activation of the macrophage. In addition to that , lipoarabinomanna also protect the bacterial from the attack of superoxide anions, hydrogen peroxide and other radicals in the body. All these mechanisms will promote the survival of bacterial in human body.
If the immune system of a person with dormant mycobacterial tuberculosis (opportunistic bacterial) in his lungs are weaken ,the infection can return back[3]. This can be causes by other disease or malnutrition. In weaken immune system state, the patients’ macrophages are unable to kill the tuberculosis bacterial, causing them continue to growth and reproduce inside the lungs and finally rupture and released out from the granuloma. This stage of infection is known as reactivation of tuberculosis bacterial. The bacterial can eventually spread to other parts of body via blood vessels and lymphatic system, thus causing infection there, this kind of infection is known as extrapulmonary tuberculosis infection[4].
In some cases ,the immune system can over respond to a minor mycobacterial tuberculosis infection, thus used up most of the body resources, and after that if another serious invasion occur ,the body immune system has no enough resources to cope and inactivate this large numbers of tuberculosis bacterial thus infection and symptoms are detected. This is known as immunopathology caused tuberculosis infection[5].
Multi drug resistance tuberculosis (MDR TB) follows the same pathophysiology above but they developed resistant to most of our first line antibiotics and stronger antibiotics are needed to kill them, example: aminoglycoside, Pyrazinamide (PZA), and antibiotic EMB6. Sometime the TB already resisted to drug before inhaled and the other time TB develop their resistance inside patient body due to mismanage of treatment. A Shanghai study shows that usually MDr.TB were caused by reinfection of a bacterial of different drug-resistant strain7.
The complications of TB are weight loss, fever, night sweat, bloody sputum and chest pain. Weight loss is due to the excessive utilization of body resources by body immune system to fight infection. Fever is caused by immune system in the fighting of TB infection.. TB bacterial releases a certain kind of chemical leading to fever as well.. During TB infection, the body temperature rises and this extra heat is released by sweating, causing night sweat. Chest pain is caused when extrapulmonary TB starts affecting lymph node beside heart(medyastinal)8.Bloody sputum proves that active TB had destroyed the alveolus and capillary around lungs.
1. Dr. Kaiser G.THE INNATE IMMUNE SYSTEM[internet].2011[modified on 2011 april;cited on 2011 august 5 ].Available from:http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit4/innate/classical.html
2. Avert group .tuberculosis[internet].2011[modified on 2011 april;cited on 2011 august 5].http://www.avert.org/tuberculosis.htm
3. Medpedia group.Extrapulmonary tuberculosis[internet].2010[modified on 2010 april;cited on 2011 august 5]].Available from http://wiki.medpedia.com/Extrapulmonary_Tuberculosis
4. Rook.G. The pathophysiology of tuberculosis .[internet].2004[2004 NOV18;2011august 5].Available from http://www.tbalert.org/resources/paper_pub/back_to_basics/rook.pdf
5. T helper cell[internet].2011[modified on 2011 July 5; cited 2011 august 5].Available from http://en.wikipedia.org/wiki/T_helper_cell
6. TB.internet.2011[modified on 2011 april 6.cited 2011 august 8].available at:http://en.wikipedia.org/wiki/Multi-drug-resistant_tuberculosis
7. Reinfection 'the main cause' of drug-resistant TB.2011[last modified 2007 april 23.cited on 2011 august 12].Available link: http://www.scidev.net/en/news/reinfection-the-main-cause-of-drugresistant-tb.html
8. Health Community .Tuberculosis
2011[2010 august 1. Cited 2011 august 12]Link:http://www.healthcommunities.com/tuberculosis/types.shtml#lym
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