Bacterial Resistance
The astounding resilience of everyday gerams has proved a major problem, one not generally anticipated. Yet, in hindsight, that germs would develop immunity to drugs should have been anticipated. Why? Consider, for example, something related that happened with the introduction of the insecticide DDT in the mid - 1940's. At that time dairymen rejoiced as flies essentially disappeard withthe spraying of DDT. But a few flies survived , and their offspring inherited immunity to DDT. Soon these flies, unaffected by DDT, multiplied in vast numbers.
Even before DDT was used, and before penicillin became commercially available in 1944, harmful bacteria gave foregleams of their prodigious defensive weaponry. Dr. Alexander Fleming, penicillin's discoverer, became aware of this. In his laboratory he watched as succeeding generations of Staphylococcus aureus (hospital staph) developed cell walls increasingly impervious to the drug that he had discovered.
This led Dr. Fleming to warn some 60 years ago that harmful bacteria in an infected person could develop resistance to penicillin. So if doses of penicillin did not kill sufficient numbers of the harmful bacteria, their resistant offspring would multiply. As a result, there would be a rebound of the disease that penicillin would not cure.
The book The Antibiotic Paradox comments: "Flemings predictions were borne out in a more devastating way than ever he surmised." How so? Well, it was learned that in some strains of bacteria, the genes - the tiny blueprints in a bacterium's DNA - produce enzymes. As a result, even extensive courses of penicillin often prove useless. What a shock this was!
In an attempt to win the battle against infectious diseases, new antibiotics were regularly introduced into medicine from the 1940's through the 1970's, as well as a few during the 1980's and the 1990's. These could treat bacteria that defiled earlier drugs. But within a few years, strains of bacteria surfaced that defied these new drugs as well.
Humans have come to learn that bacterial resistance is astonishingly ingenious. Bacteria have the ability to change their cell wall to keep the antibiotic out or to alter their own chemistry so that the antibiotic cannot kill them. On the other hand, the bacteria may pump the antibiotic out as fast as it enters, or the bacteria may simply render the antibiotic ineffectual by taking it apart.
As the use of antibiotics has increased, resistant strains of bacteria have multiplied and spread. A total disaster? No, at least not in most cases. If one antibiotic doesn't work for a particular infection, another usually does. Resistance has been a nuisance but until recently it has usually been manageable.
Next time: Multidrug Resistance
3.27.2007
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