BACTERIA & ANTIBIOTICS
Introduction
Lele (199
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Lele (1991) reports that non-response to drugs is a problem that all clinicians face. The cause may be due to resistance of the invading micro-organism or the drug used, drug dose, frequency, duration, and administration, or inadequate patient compliance. Antibiotics have been found to reduce mortality from infectious diseases, however, the prevalence of these diseases remains. It is hypothesized that use and misuse of antimicrobial agents facilitates the evolution of bacterial resistance which results in therapeutic failure. This trend is due to new resistance mechanisms and the spreading of well-characterized resistance mechanisms to the majority of bacterial species. Intrinsic resistance, or insensitivity, is described as species or genus specific; it delineates the spectrum of activity of the antibiotic. Acquired resistance is found only in certain strains of a species or genus; this results from "mutation in a gene located in the host chromosome or a plasmid or from acquisition of new genetic information by a bacterium, mainly by conjugation or transformation" (Courvalin, 1996, p. 855). Intrinsic resistance refers to a trait present in all of the members of a bacterial genus or species. However, this is a relative notion, since insensitivity can be overcome. For example, gram-negative bacteria, Enterobacteriaceae in particular, are considered naturally resistant to macrolides. Howeve
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scriptions results in resistance determinants in humans (Courvalin, 1996).
Multidrug resistance describes mechanisms of resistance by chromosomal genes activated by induction or mutation caused by exposure to antibiotics. "Exposure to a single drug leads to cross-resistance to many other structurally and functionally unrelated drugs" (p. 1). The identified mechanism involved is drug efflux by membrane transporters, many of which remain to be identified. Enteric bacteria exhibit mostly complex multidrug resistance systems regulated by operons or regulons. Enteric bacteria result in serious infections and mild gastrointestinal infections (George, 1996).
Multidrug resistance has previously been attributed to R plasmids in pathogenic bacteria; several genes in tandem on a single plasmid confer resistance to one antibiotic or several members of the same class, by enzymatic inactivation. "Antibiotics select the few resistant organisms from a largely susceptible population, invariable leading to the proliferation of resistant bacteria and consequent dissemination of resistance genes by genetic transfer among related or different species" (George, 1996, pp. 1,2).
Currently multidrug resistance is used to describe intrinsic mec
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Some common words found in the essay are:
Mechanisms Antibiotics, Findings DNA, Rybak McGrath, Conclusion Non-response, Rapoff Christophersen, Moss Musser, Gram-positive Gram-negative, Antibiotics Combination, Prescription Practices, Glickman Crawford, antimicrobial therapy, courvalin 1996, resistance mechanisms, multidrug resistance, rybak mcgrath 1996, rybak mcgrath, mcgrath 1996, patient compliance, intrinsic resistance, mycobacterium tuberculosis, george 1996, 1996 multidrug resistance, functionally unrelated drugs, cross-resistance structurally functionally, combination antimicrobial therapy,
Approximate Word count = 1930
Approximate Pages = 8 (250 words per page)
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