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Communicable Diseases: Mycobacterium Tuberculosis

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Communicable Diseases: Mycobacterium Tuberculosis Question: Discuss about the Communicable Diseases for Mycobacterium Tuberculosis.   Answer: Introduction Multidrug resistant mycobacteria infections have been the biggest challenge in microbiology and health sector. Generally, tuberculosis is a highly infectious disease caused by several species of mycobacteria, specifically the Mycobacterium tuberculosis. This condition causes many deaths because it majorly infects the respiratory system as well as many other tissues like skin, kidneys and bones in advanced stages (Lange et al., 2014). Tuberculosis is linked to many loss of lives annually via tuberculosis or tuberculosis-linked body conditions. The spread of multi drug resistant tuberculosis occurs by being spread from infected carriers (either in active or latent mode) to uninfected persons through the air. There have been high number of mortalities as a result of mycobacterium tuberculosis infection because there are some people who have no symptoms for this condition hence do not initiate treatment early enough. At this stage, there is a need for the early medication to be initiated following the positive testing by these subjects. According to Yuen et al., 2015, bearing in mind the complexity of mycobacterium species, when giving medication (specifically the antibiotics) to the patients. A big challenge however which faces the treatment process of tuberculosis is the emergence of multidrug resistant tuberculosis strains. These strains of mycobacterium undergo several rounds of mutations from time to time and hence they cannot respond to first line drugs. This challenge is faced and felt by all stakeholders including the health practitioners, communities and the government and hence the need for being addressed with due urgency (Meumann et al., 2015). Therefore, this essay explores the problems of facing the treatment of bacterial infections with focus on multidrug resistance in tuberculosis in Australia. Epidemiology The mycobacterium pathogen is passed from a person who is infected to uninfected person through sneezing and coughing, behaviors which spread pathogen droplets into the air. The pathogen is ingested by a healthy person leading to the initial infection with tuberculosis, where the pathogen spreads to several parts of the body under host immune system regulation (Trauer & Cheng, 2016). The infection with tuberculosis pathogen occurs in two steps. The first one is the latent step when the body is in a state of carrying the pathogen. The second one is the active step, where the body is unable to suppress the pathogen anymore because it is too weak. The transmission of tuberculosis pathogens occurs shortly following the patient exposuer to the active form of tuberculosis. The mycobacteria cannot be transmitted through some behaviors like sharing clothes, and bedding. This is because such pathogens die when they land on dry surfaces, as opposed to moist surfaces that they prefer in the breathing system. When the mycobacterium infectious particles are inhaled into an uninfected individual, the particle moves to the respiratory tract and lands in the alveoli. The alveoli are critical in the exchange of oxygen between the lungs, the blood and other tissues. As Subramani et al., 2017 states, although the immune system fights diseases, mycobacterium tuberculosis have cell walls that offer them protection hence they evade the immune response and are not destroyed. During normal host invasion by pathogens, macrophages are the immune cells which surround, engulf and destroy the pathogen using innate immunological mechanisms. In case a patient previously infected by another pathogen, like HIV gets exposed to mycobacterium tuberculosis, the pathogen overwhelms the immune cells and makes the body weaker than it was initially.  Active tuberculosis infection causes a widespread distribution of the pathogen from the initial site of infection, that is the alveoli, and spreads out into the blood circulation and lymphatic system. As Jenkins et al., 2014 reports, in the process, other several tissues in the body like the skin, kidneys, bones, and reproductive system become infected increasing the pathogen load in the host. The most commonly observed signs and symptoms in patients at active step of tuberculosis infection may include weight loss, reduced appetite and fever among other signs. However, it is surprising that there are some patients who are asymptomatic. As the patient sneeze and cough, they spread the infectious materials of Mycobacterium tuberculosis into the tissues, and hence more destruction of the lungs.   Screening Of Mycobacterium Tuberculosis According to Xu et al., 2017, Mycobacterium tuberculosis which is in latent step can be tested using several methods to help in early diagnosis and hence initiate early treatment. Mantoux test is able to detect tuberculosis infections as early as at two months following pathogenic infection. Mantoux or skin test involves the injection of a chemical into the skin of the forearm. If the patient develops a red wilt at the point of injection on the skin layers, then the patient is infected by mycobacterium tuberculosis pathogens. However, using the Mantoux test, it’s not possible to determine the stage of infection, that is, whether it is in latent or active step (Fox et al., 2017). Some other screening methods that can be used are x rays, and acid fact staining, which are commonly used in hospitals. The Multi-Drug Resistance Tuberculosis Having a clear understanding of the infection, diagnosis, treatment and control of tuberculosis bacteria is very important. The mycobacterium tuberculosis bacteria contain unique features from other bacteria types which makes its pathogenesis to be of special concern as argued by Kendall et al., 2017. For instance, these bacteria have high levels of lipids in their cell wall making them to resist cell wall degradation by antibiotics. The most commonly and effective test for this pathogen is the use of the acid-fast staining method for the presence absence test. It has been noted that the mycobacterium tuberculosis bacteria have a long latency period because it takes approximately 26 hours for its cell to divide, while other types of bacteria take 6 hours (short latent period) for the bacterial cells to multiply. The main reason as to why mycobacterium tuberculosis infects the respiratory system is because it is an aerobic pathogen. As a result, the lungs have a rich supply of oxygen for exchange with the respiring tissues. A number of the commonly observed multidrug resistance tuberculosis which are a global threat are as a result of errors committed by physicians while others are cause by the negligence by the patients who might fail to comply with medications. According to Tanimura et al., 2015, while nearly most countries face problems with multidrug resistance, the most affected are the developing countries due to low economic status that hinders them from effectively handling the conditions. More specifically, Shekar et al., 2014 argues that the problems of multidrug resistant tuberculosis strains are as a result of bacteria strains which have developed resistance to first line antimicrobials, rifampicin and isoniazid, common drugs used as the first line drugs in tuberculosis treatment. Molecular biology techniques have been widely used in exploring research to counter this problem and more so the manner in which multi drug resistance tuberculosis arises. Taking an example of isoniazid, drug resistance occurs when there are mutations in either the inhA or katG genes of its genetic material. For the rifampicin, drug resistance occurs when mutations develop on the beta subunit of the rpo gene on its DNA molecule (Getahun et al., 2015). In order for bacteria to be resistant to several types or classes of bacteria, there are several types of mutations which occurs in direct and indirect ways. This enables the bacteria species to switch from those that are susceptible to drugs to those that are not. During multi drug resistance tuberculosis bacteria tests, a positive standard of mycobacterium tuberculosis so that it can be used for comparison purposes. There are some other factors which would lead to development of multi drug resistant bacterial strains in tuberculosis and these include; previous medications, malabsorption and lack of proper information (Lange et al., 2014). Other minor but common cause of drug resistance could be a result of having problems poor sensitive laboratory diagnostic methods. In this case, the patients might be unaware that they possess multi drug resistant tuberculosis strains and hence may fail to get treatment as early as they are supposed to. Apart from the usual diagnostic and failure to comply with medication, there are other factors which predispose a patient to developing multi drug resistant tuberculosis as compared to another patient. A good example is a situation where a person has HIV/AIDS which in most cases makes the immune system to be weak.  In the process of making frequent visits to the hospitals, there is a higher likelihood of one developing multi drug resistance tuberculosis because their immune system is already weak. It is worth noting that the patients who have developed resistance to tuberculosis antimicrobials have only an option of using the second line agents (Kendall et al., 2017). The second line antibiotics are very expensive and are more toxic hence high mortality rates are observed especially on the patients who are susceptible to tuberculosis drug resistances.   Patient Outcomes On Multidrug Resistance Tuberculosis Once the first line agents have failed, using the second line drugs to treat tuberculosis is economically unfavorable to patients. Apart from costs, these drugs are more toxic hence raising the mortality rates among these patients, as stated by Du Toit et al., 2015. In case there is a possibility of co-infection with other diseases like cancer, HIV/AIDS or hepatitis further weakens their immune system leading to possibilities of deaths. It has been observed that patient with tuberculosis and HIV co-infection undergo poor drug malabsorption and thus high loads of the pathogen. The patients undergo other costs which may hamper treatment are high transport costs, accommodation, poor nutrition, and lack of productivity at workplaces, hence the need to alleviate them from these costs (van den Hof et al., 2016). In the event that the person is suffering from multi drug resistant tuberculosis, their low productivity means that their families are negatively affected and children may drop out of school. According to Rodrigues et al., 2017, patients who attempt to stop treatment when they feel better, need to know that the medical charges of seeking tuberculosis treatment using second line drugs are more expensive, while the toxic effects are so high as opposed to initial treatment. World Health Organization Response To Multidrug Resistance Tuberculosis The World Health Organization has recommended that Bacilli Calmette Guerin (BCG) vaccine be used in regions where tuberculosis disease is most prevalent. The BCG vaccine is made up of a weakened mycobacterium tuberculosis bacterium. Upon introduction into the body, the weak pathogen induces production of antibodies. Later on, when the actual pathogen infects the host, these antibodies will remember and mount an immunological response against the pathogen. As Roy et al., 2014 argues, although BCG vaccine has a high efficacy, it could also be affected by the geographical location of the patient as well as the age of the patient during vaccination. Other treatment methods advocated for by the World health organization are TB chemotherapy which include isoniazid, pyrazinamide, rifampicin and ethambutol (first line drugs). In case the pathogen has become resistant against these first-line drugs, then the next option is to initiate the second-line drugs on the parent. However, the second-line drugs have more serious side effects because of their low potency means that they need to be taken at higher doses.it is advisable that when tuberculosis treatment is being initiated, there is close monitoring and supervision by qualified health professionals in order to ensure drugs compliance (Manson et al., 2017). It is common that some patients may stop taking medications before the pathogen is cleared from the body. For a complete cure, it is recommended that treatment be carried out for a period of between six to nine months. There exists another method of treating mycobacterium tuberculosis infections, which is less familiar known as the DOTS-Plus technique. This technique uses a direct method of observing patients but on a short period of time. This method is commonly used in poor, rural areas where hospital facilities are not available. Development Of Multidrug Resistance To Mycobacterium Tuberculosis Multi drug resistance occurs through genetic alterations more specifically via chromosomal mutations in the genes that encode the commonly used drug targets. The accumulation of such chromosomal mutations in genes causes the insurgence of multidrug resistance (Francis et al., 2014). When this happens, the mycobacterium tuberculosis bacteria become insensitive to one or more and in this cases it is rifampicin and isoniazid. The patients who multi drug resistance bacteria strains can only rely on second-line drugs like fluoroquinolones or use injectable like kanamycin and amikacin.  Studies by Rajendran & Sethumadhavan, 2014 suggest that in order to counter multidrug mycobacterium tuberculosis drug resistance, it is vital to have a clear understanding of the basic mechanism of action of first line drugs. Here, isoniazid has been used as an example of common drugs that bacteria have developed resistance against. Isoniazid demonstrates two mechanism of action but based on the rate of bacterial cell multiplication rate. First is that isoniazid being bactericidal agents which kills bacteria in vivo within a short time, especially the fast-replicating cells. On the other hand, isoniazid acts in a bacteriostatic manner to eliminate the slow replicating bacteria strains. Since isoniazid is a prodrug, it needs to be activated in order to be catalytically active. This activation is catalyzed by the enzyme catalase peroxide homeoprotein G which then causes the blockage of mycolic acid synthesis leading to destruction of the bacterial cell walls.  Activation of isoniazid is a unique process which only occurs in mycobacterium tuberculosis pathogens leading to the formation of mycolic acid. The development of drug resistance against isoniazid by mycobacterium tuberculosis is caused by mutations in the InhA gene.   Multi Drug Resistance In Australia Tuberculosis is regarded as the most common communicable disease in the world. It is interesting to note that Austria has the lowest prevalence of tuberculosis as a result of its good public health systems. However, there are a few detected cases in the same country making the mortality rates from Australia to be at a rate of 0.6 deaths for every 100,000 people (Australian government department of health, 2016). The effects and prevalence of tuberculosis infections occur frequently among the Aboriginals in Australia as compared to other ethnic groups due to their low level socioeconomic status. This is because they have low self-esteem hence they can’t afford basic hospital service. Moreover, since they live in isolation, they do not associate with others nor seek treatment due to rich cultural beliefs. Despite the fact that Australia has for a long time recorded a low rate of multidrug-resistant tuberculosis infections, it is a predictable pattern to find that the indigenous Australians and Australians born from overseas have a higher disease burned as compared to the non-indigenous Australians. During the earliest discovery of tuberculosis in Australia, it was the leading cause of mortality and morbidity; indicating that the government has made a lot of efforts to bring the disease to control. However, Roberts-Witteveen et al., 2015 notes that as scientist struggle in microbial research and drug discovery, chemotherapy has been a scientific product which has made it possible to counter the rates of spread of tuberculosis pathogens. According to the reports from the Tuberculosis Control Program in Australia, there are major plans in place which aim at reducing the rates of tuberculosis infection as well as lower the transmission rates by use of improved tuberculosis diagnostic and treatment methods. According to James and Allen, 2016, majority of the tuberculosis infections recorded among the minority groups, a large proportion falls on the Australians who are born overseas, and the lesser proportion falls on the indigenous Australians. Examples of migrant groups in Australia who have common multidrug resistant Mycobacterium tuberculosis infections include those from Nepal, India and China. It is worth noting that according to the reports by The Australian Society for infectious Diseases, there is a possibility of previously controlled diseases re-emerging as a result of drug resistance against initially effective drugs (Pacific beat, 2016). Moreover, the Society for Infectious Diseases, warns that the development of multi drug resistant tuberculosis strains is the most common just as the cases being observed in the Queensland region.  World Health Organization recognizes that after a long period since the declaration of tuberculosis as a global health concern, there has been significant progress made to deal with its treatment. On the other hand, there has been too little progress in terms of controlling the multidrug resistant tuberculosis. The World Health Organization estimates that the overall cost of treating multidrug resistant tuberculosis is more than one hundred times more than that of those people susceptible to tuberculosis. This clearly means that there is an urgent need for the department of public health and planning to come up with more effective educative, diagnostic and treatment methods to deal with this menace before it spreads to the rest of the Australians (El-Abaseri et al., 2015). The most common toxic effects during the use of second-line agents in tuberculosis are ototoxicity and hepatitis. The side effects require that there should be more details in terms of clinical tests, monitoring and coming up with better therapeutic agents.   Conclusion In summary, the issue of multi drug resistance tuberculosis presents serious problems to the success of mycobacterium tuberculosis treatment efforts. Bearing in mind that the second line mycobacterium tuberculosis drugs are expensive and having high toxicity, there are still challenges in achieving proper treatment. Co-infection with other diseases has been found to increase susceptibility to multidrug tuberculosis infections due to weakened immune system. The ministry of health in Australia needs to formulate and implement preventive and early tuberculosis treatment programs. As these programs run, they should be closely monitored to find out whether they are actually achieving the intended purpose or not. Moreover, in Australia, it is important to lay more emphasis to the health of the Indigenous populations who in most cases are the victims of health disparities. The Australian government should also engage in campaigns, even door to door and if possible integrate screening and treatment at either affordable or no costs at all. Such efforts will make it possible to lower the transmission rates to the healthy population. By adopting these strategies, the Australian government will be able to cater for the health needs of its people who can be productive again and take care of their families without overdependence on the government provisions.   References Australian government department of health (2016). Retrieved from https://www.health.gov.au/internet/main/publishing.nsf/content/cda-cdi4003d.htm Du Toit, E., Squire, S. B., Dunbar, R., Machekano, R., Madan, J., Beyers, N., & Naidoo, P. (2015). Comparing multidrug-resistant tuberculosis patient costs under molecular diagnostic algorithms in South Africa. The international journal of tuberculosis and lung disease, 19(8), 960-968. El-Abaseri, T. B., El-Metwally, T. H., Iversen, P. L., & Adrian, T. E. (2015). Inhibition of Cytochrome P450 and Multidrug Resistance Proteins Potentiates the Efficacy of All-Trans Retinoic Acid in Pancreatic Cancer In Vitro and In Vivo. J Clin Exp Oncol 4, 1, 2. Fox, G. J., Schaaf, H. S., Mandalakas, A., Chiappini, E., Zumla, A., & Marais, B. J. (2017). Preventing the spread of multidrug-resistant tuberculosis and protecting contacts of infectious cases. Clinical Microbiology and Infection, 23(3), 147-153. Francis, J. R., Blyth, C. C., Colby, S., Fagan, J. M., & Waring, J. (2014). Multidrug-resistant tuberculosis in Western Australia, 1998–2012. The Medical Journal of Australia, 200(6), 328-332. Getahun, H., Matteelli, A., Chaisson, R. E., & Raviglione, M. (2015). Latent Mycobacterium tuberculosis infection. New England Journal of Medicine, 372(22), 2127-2135. James, M., and Allen, C., (2016). Multidrug-resistant tuberculosis in Australia and our region. EDITORIALS. Retrieved from https://www.mja.com.au/journal/2016/204/7/multidrug-resistant-tuberculosis-australia-and-our-region Jenkins, H. E., Crudu, V., Soltan, V., Ciobanu, A., Domente, L., & Cohen, T. (2014). High risk and rapid appearance of multidrug resistance during tuberculosis treatment in Moldova. European Respiratory Journal, 43(4), 1132-1141. Kendall, E. A., Cohen, T., Mitnick, C. D., & Dowdy, D. W. (2017). Second line drug susceptibility testing to inform the treatment of rifampin-resistant tuberculosis: a quantitative perspective. International Journal of Infectious Diseases, 56, 185-189. Lange, C., Abubakar, I., Alffenaar, J. W. C., Bothamley, G., Caminero, J. A., Carvalho, A. C. C., & Davies, P. (2014). Management of patients with multidrug-resistant/extensively drug-resistant tuberculosis in Europe: a TBNET consensus statement. European Respiratory Journal, 44(1), 23-63. Manson, A. L., Cohen, K. A., Abeel, T., Desjardins, C. A., Armstrong, D. T., Barry III, C. E., … & Gomez, J. (2017). Genomic analysis of globally diverse Mycobacterium tuberculosis strains provides insights into emergence and spread of multidrug resistance. Nature genetics, 49(3), 395. Meumann, E. M., Globan, M., Fyfe, J. A., Leslie, D., Porter, J. L., Seemann, T., … & Stinear, T. P. (2015). Genome sequence comparisons of serial multi-drug-resistant Mycobacterium tuberculosis isolates over 21 years of infection in a single patient. Microbial Genomics, 1(5). Pacific beat (2016). Fresh warnings over drug resistant TB in Australia and the pacific. NEWS. Retrieved from https://www.abc.net.au/news/programs/pacific-beat/2016-04-18/fresh-warnings-over-drug-resistant-tb-in-australia/7335724 Pedrosa, P., Veigas, B., Machado, D., Couto, I., Viveiros, M., & Baptista, P. V. (2014). Gold nanoprobes for multi loci assessment of multi-drug resistant tuberculosis. Tuberculosis, 94(3), 332-337. Rajendran, V., & Sethumadhavan, R. (2014). Drug resistance mechanism of PncA in Mycobacterium tuberculosis. Journal of Biomolecular Structure and Dynamics, 32(2), 209-221. Roberts-Witteveen, A., Reinten, T., Christensen, A., Sintchenko, V., Seale, P., & Lowbridge, C. (2015). Multidrug-resistant tuberculosis in New South Wales, Australia, 1999–2010: a case series report. The International Journal of Tuberculosis and Lung Disease, 19(7), 850-856. Rodrigues, G. S., Francis, A. R., Sisson, S. A., & Tanaka, M. M. (2017). Inferences on the acquisition of multidrug resistance inemph {Mycobacterium tuberculosis} using molecular epidemiological data. arXiv preprint arXiv:1704.04355. Roy, A., Eisenhut, M., Harris, R. J., Rodrigues, L. C., Sridhar, S., Habermann, S., … & Abubakar, I. (2014). Effect of BCG vaccination against Mycobacterium tuberculosis infection in children: systematic review and meta-analysis. Bmj, 349, g4643. Shekar, S., Yeo, Z. X., Wong, J. C., Chan, M. K., Ong, D. C., Tongyoo, P., … & Lee, A. S. (2014). Detecting novel genetic variants associated with isoniazid-resistant Mycobacterium tuberculosis. PloS one, 9(7), e102383. Subramani, R., Narayanasamy, M., & Feussner, K. D. (2017). Plant-derived antimicrobials to fight against multi-drug-resistant human pathogens. 3 Biotech, 7(3), 172. Tanimura, T., Jaramillo, E., Weil, D., Raviglione, M., & Lönnroth, K. (2014). Financial burden for tuberculosis patients in low-and middle-income countries: a systematic review. European Respiratory Journal, 43(6), 1763-1775. Trauer, J. M., & Cheng, A. C. (2016). Multidrug-resistant tuberculosis in Australia and our region. Med J Aus, 204(7), 251-3. van den Hof, S., Collins, D., Hafidz, F., Beyene, D., Tursynbayeva, A., & Tiemersma, E. (2016). The socioeconomic impact of multidrug resistant tuberculosis on patients: results from Ethiopia, Indonesia and Kazakhstan. BMC infectious diseases, 16(1), 470. Xu, H., Li, Y. M., Ma, H., Gu, W. T., & Chen, Z. Q. (2017). Mycobacterium tuberculosis found at both skin lesions and Mantoux testing site in a patient with erythema induratum of Bazin. The Journal of Dermatology. Yuen, C. M., Kurbatova, E. V., Tupasi, T., Caoili, J. C., Van Der Walt, M., Kvasnovsky, C., … & Ershova, J. (2015). Association between regimen composition and treatment response in patients with multidrug-resistant tuberculosis: a prospective cohort study. PLoS medicine, 12(12), e1001932.

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