Man-Made Evolution to Blame for ‘Superbug’
By J.K. Bhattacharjee and G.R. Janssen
Newspapers reported recently the death of a seventh-grade student from Brooklyn, N.Y., from an antibiotic-resistant "superbug" called MRSA, or Methicillin Resistant Staphylococcus aureus. Within the last few weeks, news media reported additional victims of MRSA and that 90,000 Americans may be sickened by MRSA this year — more than any other year to date — and that the number of deaths from MRSA in the U.S. during 2005 exceeded the number of deaths from AIDS.
It should be noted that healthy people who contract a MRSA infection can most often be treated with no serious consequences. Still, there is a problem, and it developed, we argue, from the rapid expansion and globally uncontrolled use of antibiotics.
This is a man-made resistance phenomenon that threatens our health, with no end in sight. The culprit, Staphylococcus aureus, is a common and usually harmless bacterial inhabitant of the nose and skin for many people. However, penetration of the skin can cause boils and furuncles, while deeper penetration can cause deep abscesses and toxic shock syndrome. Invasion of the blood stream can cause organ failure.
Staphylococcus aureus also can release toxins into uncooked and improperly stored or handled food. Ingestion of food contaminated with Staphylococcus aureus, or its toxins, can result in severe food poisoning within two to four hours.
Here’s why MRSA is so virile:
Penicillin, the first antibiotic, was used widely during World War II for treatment of wounded soldiers. Penicillin saved countless numbers of lives on foreign battlefields and in military hospitals.
Initially, bacteria were 100 percent sensitive to penicillin and infections were treatable with the antibiotic. By the 1960s, due to rapid expansion of antibiotic use, combined with increased production (to keep up with demand), and the exposure of large populations of fast-growing bacteria to the drug, antibiotic- resistant strains became a noticeable problem.
Decades of excessive and unnecessary antibiotic use has selected rare bacterial variants that are resistant to the antibiotic, while contributing also to the development of resistance to other antibiotics. Resistance to methicillin, a chemical derivative of penicillin, resulted from the bacteria acquiring a new gene, the product of which destroys the antibiotic, or by a mutation that altered the target of the antibiotic.
The result: The MRSA strain that is now insensitive to several otherwise clinically useful antibiotics.
Because resistance results from mutation of one of the bacterial cell’s normal genes, or transfer of a "resistance gene" from another organism, this represents a form of rapid, man-made evolution. As more antibiotics are demanded by the public (including creationists, who might refuse to accept mutation and selection as driving forces for evolution) and prescribed by physicians, more bacteria are exposed to antibiotics and selected for resistance to the drugs. Thus everyone, including patients, physicians and drug companies, is contributing to this man-made evolutionary event, with hospitals serving as the primary incubators for the generation and propagation of drug-resistant bacteria.
Young and old people are at higher risk because of immature and weakened immune systems. The cuts and bruises that school children receive relating to sporting activities, combined with frequent skin- to-skin contact and sharing of personal items, contribute additional risk. However, there are methods of prevention and treatment.
We can all maintain good skin hygiene, protect cuts and bruises, and seek rapid, complete treatment of infections with effective antibiotics. In addition, periodic disinfection of objects and surfaces in schools and hospitals should be encouraged.
And to prevent the evolution of further antibiotic-resistant strains, patients can believe their doctors when they say a cold or flu does not need to be treated with antibiotics.
J.K. Bhattacharjee is professor emeritus, Department of Microbiology, Miami University, Oxford, Ohio. G.R. Janssen is an associate professor, Department of Microbiology, Miami University.
