pick any Drug resistant strand

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Mycobacterium Tuberculosis
Mycobacterium tuberculosis is the main tuberculosis disease-causing agent. It belongs to the Mycobacteriaceae family which contains this particular species of the pathogenic bacteria. The bacteria physiology is highly dependent on oxygen which makes it relatively aerobic. As a disease-causing agent, it infects the mammalian respiratory system resulting in tuberculosis. Mycobacterium tuberculosis bacteria multiply rapidly in a time span of fifteen to twenty hours. However, its rates of bacteria multiplication are relatively slower compared to other drug-resistant bacteria such as Staphylococcus aureus. Mycobacterium tuberculosis is a multi-drug resistant pathogen (MDR)-TB that survives in the presence of tuberculosis antibiotics such as rifampicin and isoniazid. This paper will critically explain the anti-drug resistance ability of the Mycobacterium tuberculosis strand.
Over the years, tuberculosis has been one of the significant public health teething troubles worldwide. Despite the extensive research on the cure and diagnosis of the diseases, the multi-drug resistant Mycobacterium tuberculosis (MDR)-TB has proved to be a major hindrance towards finding an effective cure for the disease. In the most recent medical research, researchers have identified a more complex strain of the Mycobacterium tuberculosis which is resistant to all kinds of antibiotics; a situation referred to as totally drug resistant (TDR).

The inherent drug-resistant ability is one of the traditional molecular mechanism which makes the bacterium survive and multiply in the presence of antibiotics. The unique cell walls structure of the M. tuberculosis which contains mycolic acid gives the bacteria a relatively lower cell permeability for many compounds. This makes it possible for the bacterium to live and multiply in environments containing antibiotics and chemotherapeutic agents. Also, the efflux mechanisms of the M. tuberculosis bacteria have been attributed to its drug-resistant nature, more specifically towards antibiotics such as fluoroquinolones and tetracycline. Similarly, the bacterium inhibits psychological adaptations which have been noted to occur within the host as a factor which can be responsible for their high antibiotic tolerance.
As in the case of most drug-resistant strains, M. tuberculosis bacterium derives its antibiotic tolerance ability through acquired drug resistance mechanisms. However, for this strand, its acquired drug resistance is different from that of other bacteria which occurs through horizontal transfer of genetic elements which include, integrons and plasmids. In the case of M. tuberculosis, acquired antibiotic resistance occurs through spontaneous mutations in chromosomal genes of the bacterium. Through the chromosomal genes mutation process, it results in the production of drug-resistant strains that gives its the ability to withstand the effects of the antibiotics. However, no particular pleiotropic mutation has been identified as the major cause of the (MDR)-TB resistance in M. tuberculosis. Also, resistance to one particular drug combined with classical mutations can be stated as the initial stages of antibiotic tolerance in this bacterium (Silva, Eduardo and Palomino 1418-1420).
Medical researchers have been able to introduce new drugs to curb the multi-drug resistance in M. tuberculosis. Surprisingly, it has already been noted that the bacterium has changed to new and improved mechanisms of total drug resistance (TDR). Such antibiotic resistance mechanisms have been discovered even before the new drugs have been subjected to clinical use. Therefore, it is critically important to learn and understand the new total drug resistant (TDR) mechanisms of the M. tuberculosis to be able to find an effective cure for the highly antibiotic-resistant M. tuberculosis strand (Silva, Eduardo and Palomino 1428).
Work Cited
Almeida Da Silva, Pedro Eduardo, and Juan Carlos Palomino. “Molecular basis and mechanisms of drug resistance in Mycobacterium tuberculosis: classical and new drugs.” Journal of antimicrobial chemotherapy 66.7 (2011): 1417-1430.