Volume 1

Resistance to antibiotics and other antimicrobial agents / Select Committee on Science and Technology.

  • Great Britain. Parliament. House of Lords. Science and Technology Committee.
Date:
1998
Catalogue details

Licence: Open Government Licence

Credit: Resistance to antibiotics and other antimicrobial agents / Select Committee on Science and Technology. Source: Wellcome Collection.

    9/112 (page 7)
    1.6 We begin our report with a brief account of what resistance is and why it matters; for more on these questions, we refer the reader to arecent report by the Parliamentary Office of Science and Technology, Diseases Fighting Back (October 1994). We consider how far resistance can be controlled, and how. We then proceed to consider the evidence we have received on the various means of control: prudent use of antimicrobial agents in human medicine (Chapter 2) and in animals (Chapter 3); infection control (Chapter 4) and disease surveillance (Chapter 5); and development of new drugs (Chapter 6) and vaccines (Chapter 7). Chapter 8 considers the special problems of resistance in viruses, and Chapter 9 considers international issues including malaria. Chapter 10 considers the sources of support for research and data-collection. Our recommendations are set out in Chapter 11, and summarised in Chapter 12. Appendix 7 contains notes on some important antimicrobial agents, Appendix 8 a glossary of other terms, and Appendix 9 a list of acronyms. What is resistance? 1.7 All antibiotic resistance has a genetic basis. Some organisms are inherently resistant to many antibiotics (“innate resistance’’). This resistance probably evolved as a response to exposure to antibiotics present in the natural environment. Many such organisms pose no threat to healthy people, but may become important pathogens in vulnerable patients in hospital. Examples include the Pseudomonas species and some Enterococci. 1.8 Acquired resistance can arise by a number of diverse mechanisms: (1) Mutational resistance. These mutations have occurred randomly in a small proportion of the particular bacterial population. The most familiar example is seen in the bacterium causing tuberculosis, where a few organisms are naturally resistant to, for example, streptomycin. In the presence of streptomycin as a single antibiotic these resistant organisms soon become the dominant population. (ii) By horizontal transfer of genes determining resistance from one organism to another. This can occur by the direct transfer (conjugation) between bacteria of genetic material carried on small pieces of DNA (plasmids) situated within the bacterial cell but outside the bacterial chromosome, or by similar pieces of DNA carried on a bacterial virus, a bacteriophage (transduction), or by direct transfer of naked DNA (transformation). 1.9 | While these mechanisms have been known for many years, what has emerged more recently is knowledge of the great frequency and flexibility with which bacteria are able to exchange genetic material. and the crucial importance of these mechanisms in bacterial evolution. It is now known, for example, that genetic interchange can take place between a much more diverse variety of organisms than was formerly thought. and is probably a common event in the natural world. There is a global pool of resistance genes which can spread between different bacterial populations occupying different habitats, e.g. between man, animals and the environment. Genes carrying antibiotic resistance factors are easily able to spread if the host organism gains an evolutionary advantage in acquiring them. The importance of these processes for antibiotic resistance in man and animals is that, by whichever process genes for resistance have been acquired, the presence of an antibiotic in the environment of the bacterium imposes “selection pressure” and encourages resistance to spread. The antibiotic kills all susceptible bacteria, thereby “selecting out” the resistant strain; in this way a previously minor population of antibiotic-resistant organisms rapidly becomes dominant. Although there are enormous variations in the speed with which resistance to any antibiotic emerges, and in its geographical spread once it has emerged, it 1s indisputable that resistance has developed to many new agents after their introduction, with consequent diminution or actual loss of their former value to medicine. Thus has appeared the vicious circle repeatedly witnessed during the last half century, in which the value of each new antibiotic has been progressively eroded by resistance, leading to the introduction of a new and usually more expensive agent, only for this in its turn to suffer the same fate.