Antibiotics

After suffering a lot of devastating epidemic attacks and mass deaths, humanity invented antibiotics and started applying them against known bacterial diseases. Using antibiotics for the last 6 decades, we are now facing the results of the process caused by genetic changes and mutations in bacteria. This can be explained by one of the basic principles of evolution: natural selection, which suggests that the fittest and the strongest survive, and the weakest disappear. Bacteria are one-celled organisms, which are very vulnerable to mutations. It is known that the most of the mutations affect the organisms. But certainly, there are some chances of positive outcomes of mutations as well. Mitosis of bacteria is a very fast process, which brings to rapid growth of the population. Having such huge number of bacteria, the chances of positive mutation are higher, therefore, more and more bacteria can become resistant to antibiotics treatment. Nowadays, different types of pathogen bacteria can already survive the existing antibiotics, and using an excessive amount of antibiotics we dramatically fastened the process of natural selection in bacteria evolution. This situation threatens the effectiveness of traditional treatment methods to bacterial diseases. That is why world scientists are facing the necessity of searching for new antibiotics, either modifying the known ones or looking for something absolutely different. According to the research of the Harvard School of Public Health, in 2005 â€Å"..more than 40% of Streptococcus pneumoniae strains in the United States could resist both penicillin and erythromycin† (Powledge, 2004). The other researches, based on mathematical modeling, show that in the nearest future more and more species of bacteria will be able to resist old antibiotics. Therefore, if no new antibiotics are available, we’ll become totally unprotected against hard diseases, like tuberculosis, etc. Bibliography: Powledge, T. M. (2004, February 17). New Antibiotics—Resistance Is Futile. PLoS Biol 2(2): e53