Abstract

Antimicrobial resistance occurs when microorganisms such as bacteria, viruses, fungi and parasites change in ways that render the medications used to cure the infections they cause ineffective. This is a growing global concern because a resistant infection can spread to others, can become lethal and imposes huge costs to individuals and society.

A microorganism that develops resistance to all available antimicrobial is often referred to as superbug. Antimicrobial resistance is not a new problem but one that is becoming more dangerous; urgent and consolidated efforts are needed to avoid regressing to the pre-antibiotic era.

Consequences of Antimicrobial Resistance

•  In both humans and animals, antimicrobial resistance development will result in increased death rates and diseases because effective therapy for specific infections is delayed or unavailable. All humans and animals have populations of normal bacteria in and on their bodies. A more subtle effect of resistance on the incidence of disease occurs when a person or animal receives an antimicrobial drug to which a potentially infective or colonizing bacteria is already resistant.

Emergence of Antimicrobial Resistance

Bacteria are highly versatile in their genetic makeup and so can easily develop resistance. All bacteria have an inherent flexibility that capacitates them to evolve genes that render them resistant to antimicrobials sooner or later. Bacteria can incorporate DNA from different species and even different genera into their own genetic make-up. Also they multiply very rapidly and if the conditions are ideal they can double in 20 minutes. If even one bacteria in a billion is able to survive exposure to an antimicrobial by becoming resistant, then its descendants will quickly reproduce. The use of antimicrobials in human and animals for the last five decades has encouraged the multiplication and spread of resistant strains (Krause, R.M., 1992)

Mechanisms of Antimicrobial resistance

Two major forms of Antimicrobial resistance are mutational and transmissible. Mutational resistance occurs from chromosomal mutations in the bacterial DNA that are then transmitted to progeny during replication. This form of resistance develops slowly step by step and requires long time exposure to an antimicrobial to become clinically significant. E.g.: Clinical resistance to fluoroquinolone antimicrobials occurs from chromosomal mutations. Transmissible resistance is more rapid to develop and requires genetic exchange between bacteria.

Most of the antimicrobial resistance can be attributed to this form of resistance. Bacteria can transmit the transmissible antimicrobial resistance genes by four different mechanisms: transformation,transduction, conjugation and transposition (Murray, B., 1991)

Current Scenario in Antimicrobial Resistance

Many global trends have helped to accelerate the spread and speed of infection, including factors such as urbanisation (eg: overcrowding, poor sanitation etc), Pollution, Environmental degradation , Weather patterns (affecting the incidence and distribution of infection) , 'inappropriate' use of antimicrobials also contributes to the problem - this occurs when they are taken for too short a time, at too low a dose, at inadequate potency, or for the wrong disease, poor infection prevention and control practices . Resistance to earlier generation antimalarial medicines such as chloroquine and sulfadoxinepyrimethamine is widespread in most malaria-endemic countries. Falciparum malaria parasites resistant to artemisinins are emerging in South-East Asia; infections show delayed clearance after the start of treatment (indicating resistance). During the past 3 decades, MRSA (methicillin-resistant Staphylococcus aureus) has created significant epidemiological, infection-control, and therapeutic management challenges.

Another paper published recently by Kumarasamy et al. (2010) highlights the serious threat posed by the NDM-1 (New Delhi metallo-lactamase- 1) superbug, a microbial threat for which there is limited surveillance and no effective treatment. Western European countries have managed to decrease the rate of antimicrobial resistance in some pathogens through a multipronged approach in comprehensive well regulated health systems. Integrated monitoring of antibiotic consumption and resistance, prescriber and consumer education that is coordinated and paid for by the government and NDM-1 is a recent entrant in the family of superbugs and produces an enzyme called Metallo-beta-Lactamase-1 (MDM-1). This enzyme helps these bacteria to destroy the most potent antibiotic carbapenem, known to kill most of the known bacteria. E.coli and Klebsiella pneumoniae are the two bacteria which hosts this enzyme. MDM-1enzymes are produced by strands of DNA which bacteria are known to transfer between one another. So this superbug has the potential to get copied and transferred between bacteria, allowing it to spread rapidly. The superbug was named as New Delhi Metallo-beta-Lactamase-1(NDM-1) after the national capital (New Delhi), where a Swedish patient was reportedly infected after undergoing a surgery in 2008. Most of other patients had carried this infection from India, Pakistan and Bangladesh. regulation of use in communities and hospitals have shown that it is possible to contain antimicrobial resistance. Pharmacists readily dispense antibiotics without prescription in the developing world as their income depends on sales rather than on a professional fee or salary. Pharmaceutical companies may promote sales of antibiotics independent of patient need.

Finally, most antibiotics, by virtue of their safety and short courses, lend themselves to abuse; patients often take antibiotics of their own accord. Improved drug access without significant improvements in appropriate use will have dire consequences, with continued emergence of superbugs and untreatable infections.

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