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| LEADING ARTICLE |
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| Year : 1995 | Volume
: 41
| Issue : 2 | Page : 29-30 |
Antimicrobial resistance--a strident alarm.
R Soman
Correspondence Address:
R Soman
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 0010707703 
Keywords: Antibiotics, administration &dosage,pharmacology,Bacterial Infections, drug therapy,microbiology,Developing Countries, Drug Resistance, Microbial, Human, India, Microbial Sensitivity Tests, Risk Assessment,
How to cite this article:
Soman R. Antimicrobial resistance--a strident alarm. J Postgrad Med 1995;41:29-30 |
You may fool all the microbes for some of the time, some of the microbes all the time, but you cannot fool all the microbes all the time. When the modern era of chemotherapy of infection began in the 1930s with the clinical use of sulfonamides, infectious diseases appeared to be all conquered. The powerful arsenal of antibiotics appeared to be good, perhaps too good. They were spread around too widely, too cheaply and used indiscriminately. One result of this widespread use was the generation of antibiotic resistant organisms. Given enough time, the wily microbes learn to chew up, spit out or shield themselves from any antibiotic. This is a great disappointment but not a surprise. Microbes are in prodigious numbers and are multiplying rapidly. Every time DNA is copied, errors occur in the transcription process. Some of these, can spell disaster to many a new antibiotic. A single base change can render useless an enormous amount of pharmaceutical research effort. Such mutations of resident genes can be spread from cell to cell by mobile genetic elements such as plasmids, transposons and bacteriophages. The resistant bacteria flourish in areas of heavy antibiotic use such as hospitals and CCUs. The resistant factors can then spread far and wide through the 'internet' of bacterial populations.
When penicillin was first introduced, Staphylococci were exquisitely sensitive to it. With its widespread use, the frequency of penicillinase producing staphylococci increased. A change in the penicillin binding protein led to methicillin resistant strains (MRSA) against whom vancomycin is the only thin line of defence. Although quinolones demonstrated an acceptable activity against (MRSA) when they became first available in the 1980s, they are no longer reliably active. Organisms previously known to produce beta-lactamase occasionally such as E. coli, M catarrhalis now do so regularly. Additionally, those originally beta-lactamase negative, such as H. influenzae, and N gonorrhea are increasingly beta-lactamase producers[1]. A high rate of resistance to erythromycin and clarithromycin has been reported among pneumococci[2]. Vancomycin resistant enterococci have shown a twenty fold increase since 1987[3]. Outbreaks of cholera caused by resistant Vibrio cholerae  01 bio-type EI Tor resistant to tetracycline have occurred in Tanzania and Bangladesh[4] Shigella and Salmonella More Details resistant to the usual antibiotics are reported frequently. Klebsiella pneumoniae, which have extended spectrum beta-lactamases and aminoglycoside inactivating enzymes have been found[5]. A case of Pseudomonas nosocomial pneumonia showed a failure of treatment with ciprofloxacin, as well as with imipenam[6] Multi-drug resistant tuberculosis is raging like wild fire[7] Despite numerous attempts at eradication, malaria remains a serious endemic disease. One of the major contributing factors is the emergence of resistant plasmodia to one or more classes of antimalarial agents. The history of all antimalarial drugs has been one of initial success followed by gradual development, establishment and spread of resistance[8].
The impact of antimicrobial resistance is tremendous. It increases the morbidity, mortality and costs associated with infectious diseases. Effective therapy is delayed, particularly when resistance emerges to the drug of choice for a particular organism or to the appropriate empiric-therapy for a given syndrome. The infected person continues to transmit the resistant organisms for a longer period until an effective treatment for those organisms is used. By continuing to use the usual therapy, which is ineffective, the susceptible strains are subdued and the resistant ones are at a selective advantage. Since resistance to a particular antibiotic is often a part of a large package of resistance factors located on plasmids or transposons, simply using combinations of antibiotics in place of one may not work[9].
Developing countries have particular problems due to antimicrobial resistance. They have a heavy burden of infectious diseases and huge populations without even the rudiments of primary health care. Crowding poor sanitation and sexual contact lead to dissemination of resistant strains. Doctors working in developing countries seem to see as many patients as possible in the shortest time without laboratory and radio-logic support. They are compelled to prescribe antimicrobials to meet patient expectations 2. and inappropriate use of them is a common phenomenon[10].
Antimicrobial drug resistance will continue to pose a challenge in future. Accurate diagnosis and susceptibility testing will become increasingly important. Knowledge of local susceptibility patterns and increased support from the microbiologic laboratory will be crucially important. The solutions to all these problems require more than just scientific breakthroughs. Patients must not make unreasonable demands for antibiotics, nor should doctors prescribe them, when none are indicated. Once antibiotics are started, the course should be completed, especially with regard tuberculosis. Rapid, accurate methods of diagnosis to confirm or exclude an infective cause are needed. Development and use of antimicrobial agents with a more discriminant, narrow spectrum is encouraged. Intensive infection control measures including simple ones like hand washing and good sanitation are a must. However it must be realised that much in today's world works against the very principles of infection control.
| :: References | |  |
| 1. |
Sensakovic JW, Smith LG. Beta-lactamase inhibitor combinations. Med Clin North Am 1995; 79:695-704.  |
| 2. | Lonks JR, Mederios AA. High rate of erythromycin and clarithromycin resistance among S pneumoniae isolates from blood cultures from Providence, Rhode island Antimicrob Agents Chemother 1993; 34:1742-1745. |
| 3. | Nosocomial enterococci resistant to Vancomycin - United States 1989-1993 MMWR 1993; 42:527-596. |
| 4. | Kiien NC, Cunha BA. Tetracyclines. Med Clin North Am 1995; 79:789-801. |
| 5. | Smith CE, Tillman BS, Howell AW. Failure of ceftazidime amikacin therapy for bacteremia and meningitis due to Klebsiella pneumoniae producing extended spectrum beta-lactamase. Antimicro Agents Chemother 1990; 34: 1290-1293. |
| 6. | Fink MP, Synman DR, Niederman MS. Treatment of severe pneumonia in hospitalised patients: results of a multi-centres, randomised, double-blind trial comparing intravenous ciprofloxacin with imipenem-cilastatin. Antimicrob Agents Chemother 1994; 38:547-552. |
| 7. | Peloquin CA. Multi-drug resistant Mycobacterium tuberculosis. Med Clin North Am 1993; 77:1253-1262. |
| 8. | Palmer KJ, Holiday SM, Brogden RN. Mefloquine Drugs 1993; 45:430-475. |
| 9. | Tomasz A. Multiple antibiotic resistant pathogenic bacteria. A report on the Rockfeller University Workshop. N Engl J Med 1994; 330:1247-1251. |
| 10. | Kunin CM. Resistance to antimicrobial drugs - a wide calamity, Ann Int Med 1993; 118:557-561.
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