The rise in bacterial resistance
Bacteraemia and antibiotic resistance of its pathogens reported in England and Wales between 1990 and 1998: trend analysis
The rise in antibacterial resistance is partly because there have been no new classes of antibiotics introduced since the 1960s reports Professor Sebastion Amyes in an editorial this week's BMJ.
We now know, due to improved surveillance methods, that antibiotic resistance is rising inexorably (see also, paper by Reacher et al in the week's BMJ), says Professor Amyes from the University of Edinburgh. However, it has taken a long time to ascertain the extent of the problem and we still have a lot to learn about the mechanisms through which antibiotic resistance develops, he explains.
In his editorial Amyes quotes the surgeon general of the United States at the end of the 1960s as saying that "we could now close the book on infectious diseases". "At the start of a new century, some 30 years later…we are facing a potential treatment crisis for some infections," says Amyes and this may be partly due to the fact that no new clinically useful structures of antibiotics were discovered after 1961. Almost all the drugs that have been launched since the 1960s have been modifications of antibiotics we already have, he says. He explains that this means that bacteria that had "learnt" how to resist one member of a chemical drug class, did not have to learn much more to overcome later modifications.
The author also considers the role that the introduction of organ transplantation has played in antibiotic resistance (aggressive antibacterial therapy was required to protect immunosuppressed patients against hospital acquired infections). He also speculates that multiresistant bacteria may have been facilitated by hospital designs that move patients closer together and rely on regular movement of patients around the hospital for their different points of treatment.
Amyes concludes that as our knowledge of molecular biology increases and the bacterial genome projects advance we will obtain a greater understanding of resistance and the mechanisms through which it works.
Contact:
Professor Sebastian Amyes, Professor of Microbiology, Medical School, University of Edinburgh
Email: s.g.b.amyes@ed.ac.uk
Reacher et al can be reached through Simon Gregor, Press Office, Public Health Laboratory Service, London
Tel: 0181 200 6868 x4097
Fax: 0181 200 8130
Email: sgregor@phls.co.uk