Mohemid, Do you want to use antibiotic resistance patterns as a tool in epidemiology (studying outbreaks, tracing back nosocomial infections) or are you interested in monitoring patients under therapy?

Antibiotic resistance patterns as epidemiological markers are just a very basic measurement. If two isolates are compared and the resistance differs, these isolates may be unrelated. However, if one compares two isolates of, for instance, Enterobacter cloacae, one may be susceptible and the other one resistant to beta-lactams. Are they of different origin? Not necessarily. Since E. cloacae mostly carries ampC genes, which can easily be induced to be hyperproducers, the two isolates may have the same ancestor (i.e. are epidemiologically linked). One isolate could have been obtained from a patient without antibiotic therapy, the other one after therapy.

The other way round may also give misleading results. If you think about two isolates which share the same antimicrobial resistance pattern, this does not judge for the conclusion that they are indeed identical (epidemiologically linked). The resistance pattern observed may just be a very common one, thereby raising the chance, that two unrelated isolates share the same pattern.

For this reason antimicrobial resistance patterns are just a very basic but potentially misleading tool for epidemiology. Therefore, if you use resistance patterns for epidemiology studies, you should be aware about the limitations. For studying relatedness of isolates, molecular methods are more appropriate. However, although frequently used, even molecular methods like PFGE may not always be sensitive enough to reliably discriminate two isolates.

Resistance patterns may be helpful in monitoring therapy of patients. If resistance is monitored on a longitudinal axis, than changes in resistance may guide the clinician when to adapt therapy.

Hope the answers helps. Best regards, Oliver

Generally in the antibiotic treatment depends on the disease in question, usually we (the perfect protocol must be by step) With first-choice antibiotics are prescribed, Depending on the evolution and / or worsening of the patient, The Medic decides to opt for antibiotic of second generation, to finish in third generation broad spectrum antibiotics ie, the problem of antibiotic resistance the Beginning When the protocol is skip from the first step to 3th step , medicating a common diseases with antibiotic of third generation, this is the root of resistance to the antibiotic. By the way is a common problem in countries in process of development

Please review few references below:

The changing epidemiology of resistance. Antimicrob. Chemother. (2009) 64 (suppl 1): i3-i10. doi: 10.1093/jac/dkp256

Peter M. Hawkey1,2,* and Annie M. Jones3

Abstract

Antibiotic resistance is now a linked global problem. Dispersion of successful clones of multidrug resistant (MDR) bacteria is common, often via the movement of people. Local evolution of MDR bacteria is also important under the pressure of excessive antibiotic use, with horizontal gene transfer providing the means by which genes such as blaCTX-M spread amongst different bacterial species and strains. β-Lactamase production is a common resistance mechanism in Gram-negative bacteria, and the rapid dissemination of novel genes reflects their evolution under the selective pressure of antibiotic usage. Many Enterobacteriaceae now carry broad-spectrum β-lactamases such as CTX-M, with particular genotypes associated with different geographical regions. The spread of these enzymes has compromised the clinical utility of a number of β-lactam classes and with the spread of genes such as blaKPC, carbapenems may be increasingly compromised in the future. High-level fluoroquinolone resistance (mainly caused by gyrA mutations) has also been shown to be associated with CTX-M and CMY-type enzymes, commonly due to co-carriage on conjugative plasmids of the gene for the aminoglycoside-inactivating enzyme AAC-61-Ib-cr and qnr genes (which confer low-level resistance), allowing the easy selection of gyrA mutants in the host strain. Resistance in Gram-positive bacteria is also widely distributed and increasing, with the emergence of community-associated methicillin-resistant Staphylococcus aureus (MRSA) blurring the distinction between hospital and community strains. Antibiotic use and environmental factors all have a role in the emergence and spread of resistance. This article reviews some of the new mechanisms and recent trends in the global spread of MDR bacteria.

Intensive Care Med. 2000;26 Suppl 1:S14-21.

Epidemiology of antibiotic resistance.

Livermore DM1

Abstract

Three biological processes contribute to the accumulation of bacterial drug resistance: new selection, gene epidemics and strain epidemics. New resistance emerges by (i) the advantaging of entire species, (ii) by mutation, and (iii) by the escape of resistance genes to mobile DNA. Organisms to have 'benefited' from modern patterns of cephalosporins and quinolone use include enterococci, Clostridium difficile, coagulase-negative staphylococci and Enterobacter spp. Mutational resistance notoriously occurs with certain antibiotic/organism combinations and allows rapid multifocal accumulation of resistance. At worst, therapy can fail when resistant mutants are selected in individual patients. Escape of new genes to mobile DNA is rare but, having occurred, permits massive 'gene epidemics', as the same genes and plasmids spread into diverse pathogens. Strain epidemics notoriously occur in individual units, reflecting break-downs of hygiene. Some strains achieve a much wider distribution: thus, much of the MRSA problem in the UK depends on the dissemination of two epidemic strains, EMRSA15 and 16; penicillin resistant pneumococci of serotypes 6 and 23 have disseminated internationally from Spain and a serotype K25 strain of Klebsiella pneumoniae with SHV-4 beta-lactamase has spread widely in France. It remains unknown why some strains and genes achieve wide spread whereas others, equally resistant, fail to do so. There is no simple cure for resistance but the best opportunities for control lie in lesser and better use of antibiotics backed by swifter and more accurate microbiology; in developing new antibiotics; and in protecting old ones from resistance determinants. All this must be supported by good local knowledge of the epidemiology of infections and resistance and of the likelihood of particular antibiotics to select resistance.

Int J Antimicrob Agents. 2008 Nov;32 Suppl 1:S2-9. doi: 10.1016/j.ijantimicag.2008.06.016. Epub 2008 Aug 30.

The epidemiology of antibiotic resistance.

Gould IM1.

Abstract

Antibiotic resistance has reached crisis point in many hospitals around the world. The majority are swamped with meticillin-resistant Staphylococcus aureus (MRSA), and many with multidrug-resistant (MDR) Gram-negatives. Whilst there are good treatment alternatives available for serious infections due to MRSA, mortality rates remain high. For MDR Gram-negatives the situation is more complex and worrying. There are few, if any, new agents in development that can be expected to benefit the situation in the next decade. Moreover, extreme (or extensive) drug-resistant and even pandrug-resistant Gram-negative infections are increasingly being described. Although definitions are confused in this area, reports suggest that patients in some intensive care units are dying from lack of availability of any antibiotic active against certain strains of Pseudomonas aeruginosa and Acinetobacter baumannii. A better understanding of the molecular basis of resistance is urgently needed if it is to be successfully overcome. Moreover, we urgently need better global early warning systems to detect new resistances and put mechanisms in place for their control.