The war against germs….Biswaroop Chatterjee
It could easily turn against us without antibiotic stewardship
It could easily turn against us without antibiotic stewardship
Do you know of a relative or a friend who died of typhoid? Or tuberculosis? Or fever after childbirth? Not very likely, unless you were born before the 1940s. The discovery of the sulfonamides in 1936, then penicillin and streptomycin in the 1940s, and then a whole range of cillins and mycins and floxacins from the 1950s onwards changed all that by letting us treat most common infections.
Our victory over germs has never been a cakewalk because bacteria become resistant to any widely used antibiotic with remarkable alacrity. For example, most strains of Staphylococcus aureus (a nasty germ that can infect almost any part of the body) were sensitive to penicillin when that antibiotic was first introduced in 1943. By 1950, 40 per cent of hospital-acquired strains of staphylococcus in the US were resistant to penicillin; by 1960 this figure went up to about 80 per cent. Fortunately, methicillin, a chemically modified form of penicillin, came in the late 1950s to save the day for us.
Lets take a quick look at how bacteria develop resistance. To begin with, most antibiotics are natural compounds (or their derivatives) that are produced by soil-dwelling bacteria in minute quantities as biological weapons. Bacteria that have been exposed to such compounds for millions of years have evolved ways to resist their lethal effects. When we produce the same antibiotics by the tonne and spread them all over the world, we give the naturally resistant bacteria a chance to flourish at the expense of the sensitive bacteria, which are killed off by the antibiotic. When the naturally resistant bacteria come in contact with disease-causing bacteria, they sometimes swap their antibiotic-resistance genes. Many bacteria are not choosy about where they get their genes from. Add to that the fact that bacteria can divide as often as once every 30 minutes, copying their DNA every time they divide, with each copy of DNA having a random chance of acquiring copying errors (a.k.a. mutations) and you have the perfect recipe for every possible combination of genes on the planet.
So, the typical sequence of events has been like this: a new antibiotic comes in the market, bacteria become resistant to it in several years time, then a newer antibiotic comes on the block. It has been a win-win situation for all parties concerned: patients and doctors are happy because infections continue to be treatable; the pharmaceutical industry is happy because their newly discovered antibiotics sell at a premium.
Now, if bacteria have been developing resistance to antibiotics all along, then why the commotion over the germs that produce the newfangled enzyme called New Delhi Metallo-beta-lactamase-1 (NDM-1)? Well, part of the reason is that NDM-1 makes bacteria resistant to an extremely useful group of antibiotics called the carbapenems. The carbapenems, while frightfully expensive, are able to kill a remarkably wide range of bacteria. They are like machine guns: no need to aim, just shoot. Besides, the bacteria producing
NDM-1 are automatically resistant to all penicillin derivatives and cephalosporin derivatives. Many NDM-1-producing bacteria are simultaneously resistant to most other antibiotics, except the polymyxins and tigecycline. The polymyxins are extremely toxic and tigecycline is expensive, so it is really Hobsons choice. Besides, we are now face-to-face with the uncomfortable question: after tigecycline, what?
New drug discovery has failed to keep pace with the development of antibiotic resistance over the last two decades, especially for Gram-negative bacteria, a group that includes E. coli, Salmonella typhi and many other well-known germs.
Where do we go from here? The only option is antibiotic stewardship. The best of antibiotics will lose all clinical utility unless used judiciously.
Antibiotic stewardship mainly consists of using antibiotics as sparingly as possible. And there are many ways to go about it:
a) Many infections do not call for antibiotics at all. For example, most episodes of sore throat in adults are caused by viruses where antibiotics are worse than useless because the risk of drug-allergy and antibiotic-associated diarrhoea outweigh the nonexistent advantages.
b) Avoid polypharmacy. If a patient has uncomplicated malaria, treat with antimalarials only; no need to add an antibiotic.
c) Antibiotics are not needed after a lot of planned surgery on clean sites; at the most, use two doses.
d) Keep some drugs strictly in reserve for desperate emergencies when other drugs dont work and only on the advice of an infectious diseases specialist.
When antibiotic-resistant bacteria are detected, utmost caution is to be taken to prevent them from spreading. That does not require rocket science; standard hygienic procedures developed over the past hundred years are good enough.
And if all this sounds utopian, let us remember that countries like Sweden and the Netherlands have been able to maintain the efficacy of old and inexpensive antibiotics such as penicillin and amoxicillin by these means till today. The system requires money to run, but that is offset by the money saved on expensive antibiotics, and the lives saved from untreatable infections.
The writer is a microbiologist, express@expressindia.com
URL: http://www.indianexpress.com/news/the-war-against-germs/775831/0