The global increase in resistance to antimicrobial drugs, including the emergence of bacterial strains that are resistant to all available antibacterial agents, has created a public health problem of potentially crisis proportions.
American Medical Association, 1995
Box 14.6 Where did antibiotic resistance come from?
Have genes responsible for antibiotic resistance always existed in nature, or have they arisen since the development and widespread use of antibiotics? The answer, almost certainly, is the former. A sample of an E. coli strain, freeze-dried in 1946, was revived many years later, and found to have plasmid-encoded genes for resistance to streptomycin and tetracycline, neither of which were in clinical use until some years after the culture was preserved. It seems likely that bacteria possessed these genes to protect against naturally occurring antibiotics, an idea supported by the fact that R-plasmids have been found in non-pathogenic soil bacteria. Also, resistance to a number of antibiotics has been demonstrated in soil and water bacteria from sources sufficiently remote to be free from anthropogenic influence.
As we have already suggested, the impact of certain antibiotics can be greatly reduced due to the development of resistance by target pathogens (Box 14.6). This represents the greatest single challenge facing us in the fight against infectious diseases at the start of the 21st century. Fleming himself foresaw that the usefulness of penicillin might become limited if resistant forms of pathogens arose.
Not long after penicillin was put into general use, strains of Staphylococcus aureus were found which did not respond to treatment, and by 1950 penicillin-resistant S. aureus was a common cause of infections in hospitals. A decade later, a semi-synthetic form of penicillin, methicillin, was introduced; this was not affected by the ft-lactamase enzymes that inactivated Penicillin G, and was used to treat resistant forms. Within years, however, came the first reports of strains of S. aureus that did not respond to methicillin. The incidence of methicillin-resistant S. aureus (MRSA) has increased greatly since, and it represents the major source of nosocomial infections. In 1980, synthetic fluoroquinolones were introduced to counter the threat of MRSA, but within a year 80 percent of isolated strains had developed resistance to these too. Vancomycin is regarded as a last-resort treatment for MRSA, for a number of reasons; it has a number of serious side-effects, its widespread use would encourage resistance against it, and it is extremely expensive.
A case of vancomycin-resistant Staphylococcus aureus (VRSA) emerged in Japan in 1996; a few months later it had reached the USA. This represents a serious threat; some of these strains respond to treatment with a cocktail of antibiotics, but already people have died from untreatable VRSA infections. In 2003, a strain of VRSA was shown to have obtained its vancomycin resistance by cross-species transfer from a strain of Enterococcus faecalis.
Nosocomial infections are ones that are acquired in hospitals or similar locations. Some 5--10 percent of hospital patients acquire such an infection during their stay. This may prove to be fatal, especially among the elderly and immuno-compromised. As well as the human cost, such infections extend the average time spent in hospital and therefore add greatly to the costs of treatment.
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