Initial protection against tuberculosis is achieved through the BCG vaccine which is administered at birth. This vaccine is expected to last up to 15 years. Even with the availability of this vaccine, tuberculosis remains a more devastating disease than ever. While only a week or two of monotherapy is needed to cure most bacterial infections, to successfully cure tuberculosis, at least 6 months are needed using a broad range of antibiotics to combat uncomplicated drug-susceptible tuberculosis, with a 90% cure rate. no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Since 1994, the same four drugs (isoniazid, rifampin, pyrazinamide, and ethambutol) have been used as the first step in treating tuberculosis. However, factors including prolonged treatment time and patient noncompliance have led to the emergence of drug-resistant tuberculosis strains such as XDR-TB that, at a minimum, are resistant to isoniazid and rifampin. This multidrug-resistant strain requires at least 20 months of treatment with toxic drugs and with a reduced cure rate of 60%-75%. In the 1990s, research into developing drugs against tuberculosis stopped. The ability of first-line drugs to cure tuberculosis and the fact that most new cases are found outside developed countries have led to a decline in overall incentives for investment in the development of new anti-tuberculosis drugs. resistance in tuberculosis has brought attention back to once-neglected strategies to improve tuberculosis treatment. One reason mycobacteria has strangely high antimicrobial resistance may be due to the unique complexity of its cell wall. It contains a complex network of macromolecules including mycolic acid (MAgP complex) which allows Mycobacterium tuberculosis to be impervious to techniques such as Gram staining. this, along with arabinogalactan, peptidoglycan, and various other proteins and polysaccharides combine to form the main scaffold of the mycobacterial cell wall. Forming an incredibly high barrier for antimicrobial agents to cross. Antimicrobial peptides (AMPs) represent a new treatment strategy against tuberculosis that can overcome cell wall protection. One of the main mechanisms of AMP interactions is their ability to completely disrupt the cell membrane or create transient pores. The first step of the interaction between AMPs and the bacterial cell is the mediation of their positive charge to bind to the negatively charged prokaryotic cell surface. The binding between cationic AMP residues and the anionic cell surface of the cell encourages the membrane to become more permeable. This allows many AMPs to apply a killing mechanism through destruction of the cell membrane. Despite the direct killing mechanism exerted by antimicrobial peptides, as well as their immunomodulatory properties, AMPs still face major challenges when it comes to entering the pharmaceutical industry. Some of the major drawbacks of using AMPs in anti-tuberculosis strategies include the high cost of synthesis, low stability in human biological fluids, and the potential for tumorigenesis and angiogenesis as side effects when administered at high concentrations. However, the long list of advantages of this type of therapy, including multifunctionality, rapid direct killing mechanism and synergy with current antibiotics, show.