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Tuberculosis might not be the most feared disease in the United States because it's well controlled and routinely tested for. But in low sources countries like the sub Sahara in Africa tuberculosis is becoming the number one cause of death. The role Bacille Calmette Guerin (BCG) vaccine is partial and the treatment methods used now are date way back in history. The spread of HIV in these low sources countries is helping the spread of TB and making it more and more resistance to multi drug treatments. A world wide plan to fight TB is needed but such a plan requires many efforts and resources. The following paper collects data from five year between 2001 and 2006, from reliable databases. The purpose of it is to connect all the studies that been done about TB and its connection with HIV. TB has caused an epidemic worldwide, and the latest data about it was collected in 2004 where it showed increase in Africa and stabilization or even a decrease everywhere else. The increase in Africa is related to the HIV epidemic there. The risk of TB is doubled with in the first two years of HIV which leads to the reactivation of the latent form on TB. Multidrug resistance TB is increasing because the treatment for it is long and costly. Also extensively drug resistance TB is developing which resists almost every TB drug out there and it makes 24% of all multidrug resistance TB. Thus a new antimycobacterial drug is needed and more cautious with handling individuals with multidrug resistance TB. The relation between the pathogen and its host lasts for decades in which the pathogen lives inside the macrophages and can make changes to its genome and evolve to a stronger pathogen. Genomic studies on different kinds of TB pathogens suggested that they have a common ancestor and immigrated with humans thus spreading in different regions of the world and adapting to different populations via mutations.
TB pathogens have different mechanisms in which they increase their virulence. Some are known for the production of immunosuppressive glycolipid, others are capable of weakening the immune system via a phenotype which leads to a greater spread in populations. The cell wall of the mycobacteria its self contains many components which cause adjustment of the immune system. These components trigger immune response by binding to tool like receptors on macrophages and dentritic cells which turn on an immune response and cause T-cells to produce interferon Î³ cytokines which alert other immune cells to be turned on. The exact mechanism in humans is still unclear; however vitamin D is activated as a result of this mechanism thus opening new doors into looking in the role of vitamin D in fighting TB. Many defense mechanisms are used by the body against mycobacteria . Autophagy is one in which mycobacteria is taken up into the endoplasmic reticulum, another is the recognition of mycobacteria antigens by T-calls on dentritic cells surface after they engulf apoptotic macrophages. Or via the antimicrobials releases by neutrophils into the macrophages that contain the mycobacteria. Another way of fighting TB by the immune system is cytokins which trigger the activation of immune cells. TB has many ways to suppress the immune system by T-cell apoptosis or escape it by bacterial membrane proteins, small molecule transporters or the ability to switch source of energy depending on the conditions. Microscopy, flurescent microscopy, liquid culture, smear and nucleic acid amplification are few possible tests to detect the presence of TB. TB has two distinguish proteins that stimulate T-cells and the release of interferon Î³ cytokins thus making the bases for many of TB detection tests. But false results are easily obtained due to the similarity of these proteins in BCG and other mycobacteria. A more sensitive assay is the ELISA spot, and although ELISA doesn't differentiate between active from latent but diagnoses could be based on the site of the infection. Easier and more accurate tests are in development to be able to detect TB in HIV patients. The best way to detect multi drug resistance TB is by microscope analysis or testing if a TB infection resistance to rifampisin which is one of the strongest TB medications. Treatment for TB is very long and hard to keep up with. The treatment is made of cocktail of drugs and last for 6 month. Programs needed to be put in place to make sure the treatment is being strictly followed to prevent the evolution of drug resistance TB because people tend to stop the treatment when they start feeling better. The DOTS (directly observed treatment short course) strategy has been developed to follow up with TB patients and try to ensure the completion of the treatment, but this strategy is costly in under developing countries where TB is most spread. To get around that studies are in progress to develop a long lasting drug that could be administered lesser times in a longer range of time, but TB has acquired resistance to some of these drugs like rifapentine in HIV patients. Thus higher doses are being studied in hope of a new strategy to fight TB. Many new drugs have been mixed with some of the older once in cocktails and showed promising results in vitro and vivo but is still needed to be confirmed in clinical trials. Many concerns come with the developing of new drugs like the possibility of resistance developing against it or toxic effects on humans with higher dosages. Pulmonary cavitation is observed in adult TB but not in HIV infected patients thus leading to the conclusion that a well functioning immune system is responsible for it. Also paradoxical deterioration which is the reappearance of the Tb lesions of new TB lesions after treatment, make the treatment harder specially after it has been frequently observed in HIV patients. These observations lead to the concentration of immune targeted therapy to try to strengthen the immune system to fight TB. Some clinical trials are being run on interferon Î³ inhalation which is a cykotine that plays a part in T-cells activation in the immune system. Another trial is about vaccination with dead M vaccae which is a kind of mycobacteria that non pathogenic but is similar to TB that is found in the environment. The idea is to the vaccine with M vaccae will stimulate the immune system to create a response to it thus creating memory cells that would better attack TB in the future due to the similarity. The research has come to the conclusion that this vaccine didn't make any difference in the death rate due to TB and thus failing as a potential treatment for TB. Steroid treatment for HIV infected patients has shown to increase the HIV viral amount thus leading to further concerns in treating with steroids. Latent TB is harder to detect and so far the most efficient successful test for it is the skin test.
People who test positive for it have the option of going on 6-12 moth treatment to clear out their system but despite the preventive therapy TB which resistance to the preventative drug treatment could still occur. The BCG vaccination varies in how long its protection lasts and it has been found that it doesn't play a part in protection against TB transmission. Thus a need for better vaccination lead to the development of many vaccinations which some have made it to clinical trials as of now. Vaccination after the infection with TB has also shown to decrease the chance of reactivation. But just as new drugs problems also face TB vaccination. One of the concerns is the long period of time a patient has to be followed up with to confirm the effectiveness of the vaccine which could be up to several years. A second concern is the indefinite knowledge about the immune system response and its components role in fighting TB since it can't be applied in vitro. Meanwhile new therapies are being worked on, HIV associated TB is growing and an action is needed immediately. The best solution as of now is the treatment of both HIV with antiretroviral drugs and treatment of latent TB with preventive drugs. But the administration of both treatments at the same time is that easy due to the toxic effect of drug interaction which leads to immune reconstitution inflammatory syndrome which is hard to detect in TB patients due to the similarity in lung Xray which could be mistaken with immuopathological immunity to TB. For now Tuberculosis and HIV is an alarming problem that is causing epidemics especially in the sub-Sahara Africa. The combination of these two diseases is helping the bacteria to grow stronger and more resistance to already developed treatments. Although this is becoming a global issue but since too much effort is needed to deal with it globally, regional action is needed to try to put a limit to this epidemic. Overall this seminar is too broad and full with overwhelming data to try and give a general idea of what is going on in the TB/HIV world. Many more details and research is needed and mostly updates on many experiments to see if they were proven good or not useful. Many experiments where labeled as not reliable without looking for the details reasons behind why so. Learning why something doesn't work helps us find new ways in which new treatments might work. Work cited â€¢ De Bruyn Guy, Garner Paul. Mycobacterium vaccae immunotherapy for treating tuberculosis. Cochrane Database of Systematic Reviews: Reviews 2003 Issue 1 John Wiley & Sons, Ltd Chichester, 2003. â€¢ Tuberculosis. By: G. Maartens & R.J. Wilkinson. The Lancet. 2007. Vol. 370(9604).