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Bacteria reproduce by mitosis to create clones. How did extremely drug resistant tuberculosis ever evolve?

Tuberculosis (TB or tubercles bacillus) is a disease caused by an infection with the bacteria Mycobacterium tuberculosis. Estimates suggest that approximately one third of the worlds population is currently affected by various strains of mycobacteria, with about two million deaths occurring annually, despite prevention efforts through the Bacillus Calmette-Gurin (BCG) vaccine and screening programmes. The majority of instances are of a latent infection (asymptomatic i.e. it exists in the absence of typical symptoms e.g. chronic cough with blood-tinged sputum, fever, night sweats, and weight loss). TB usually targets the lungs but is well known to attack other areas as well (extra-pulmonary tuberculosis). After diagnosis by a number of methods such as radiology or a tuberculin skin test, the main course of treatment follows. This nearly always includes the usage of antibiotics, primarily rifampicin and isoniazid. As a result of their use, in spite of precautions taken, multi-drug-resistant tuberculosis and extensively drug-resistant tuberculosis have, unfortunately, developed. Often, the active TB disease is best treated with combinations of several antibiotics, to reduce the risk of the bacteria developing antibiotic resistance. Drug resistance is a common occurrence nowadays with a range of diseases, Methicillin-resistant Staphylococcus aureus (MRSA) being a very famous example in the United Kingdom. Drug-resistant tuberculosis is transmitted in the same way as standard TB. Primary resistance occurs in people infected with a resistant strain of TB. A patient with fully susceptible TB develops secondary resistance (acquired resistance) during TB treatment due to inadequate therapy, failing to take the prescribed regimen appropriately, or using substandard prescription medication. Drug-resistant TB is a public health crisis in numerous developing countries, as treatment is prolonged and requires more costly drugs. Multi-drug-resistant tuberculosis (MDR-TB) is distinguished as resistance to the two most effective first-line TB drugs: rifampicin and isoniazid. Furthermore, extensively drug-resistant TB (XDR-TB) is o possibility where resistance to three or more of the six classes of second-line drugs is present. The principal source of antibiotic resistance is genetic mutation in bacteria. As soon as there is a single resistant strain of bacteria, due to the fact that it reproduces by mitosis, its offspring will be genetically identical to it (clones) and will, therefore, be resistant to the particular drugs used initially. Hence, the number of resistant bacteria will increase and the initial drugs utilised will be References: - ;

rendered redundant. The prevalence of antibiotic resistant bacteria is a consequence of antibiotic use both within medicine and veterinary medicine. The greater the duration of exposure, the greater the risk of the evolution of resistance, irrespective of the severity of the need for antibiotics. Moreover, research has shown that the bacterial protein LexA may play a key role in the acquisition of bacterial mutations giving resistance to quinolones and rifampicin. As resistance becomes more widespread, there becomes an increased need for alternative treatments. Nevertheless, in spite of a surge for new antibiotic therapies, there has been a continued decline in the number of newly approved drugs. Antibiotic resistance, therefore, poses a significant and formidable problem.

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