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S, susceptible; I, intermediate; R, resistant.

The values show MIC in mg/l, in accordance with the recommendations made by the NCCLS (National Committee for Clinical and Laboratory Standard) for each year of reference for Pneumococcal Pneumonia, defining the standards for susceptibility, intermediate resistance and resistance (NCCLS, 1999; NCCLS, 2000; NCCLS, 2002).

S, susceptible; I, intermediate; R, resistant.

The values show MIC in mg/l, in accordance with the recommendations made by the NCCLS (National Committee for Clinical and Laboratory Standard) for each year of reference for Pneumococcal Pneumonia, defining the standards for susceptibility, intermediate resistance and resistance (NCCLS, 1999; NCCLS, 2000; NCCLS, 2002).

of resistant organisms. Alexander Fleming first noted that certain bacteria, such as Haemophilus influenzae, were naturally resistant to penicillin, but the real significance of resistance emerged as penicillin was used to treat serious staphylococcal infections. Whereas before 1946 about 90% of Staphylococcus aureus isolates in hospitals were susceptible to penicillin, 75% of isolates were resistant by 1952 (Findland, 1955). The first decade of the clinical use of the sulfonamides also saw the widespread emergence of resistance to these drugs in several gram-negative bacteria (Coburn, 1949; Woods, 1962). At that time, the close relationship between the use of low dosage antibiotics and the later appearance of resistance had already been proven and described by Fleming, in relation to S. pneumoniae resistance to sulphamides, and later by Chain, with reference to the appearance of penicillin resistance (Florey, 1943; Maclean and Fleming, 1939).

Bacteria can evade antimicrobial action by adopting diverse mechanisms. These mechanisms include enzymatic inhibition, altered porin channels, alterations of outer or inner membrane permeability, modification of target proteins, antibiotic efflux, and altered metabolic pathways. Intrinsic resistance is a naturally occurring phenomenon that occurs in the absence of antimicrobial selection pressure. It occurs in all members of a genus or species and the term implies that not all species are intrinsically susceptible to all antimicrobials. Acquired resistance may be permanent or temporary or "adaptative" (dependent on the growth conditions). Permanent resistance arises either from mutations (chromosomal resistance) or from acquisition of DNA from an outside source by one of three distinct mechanism: (a) transduction (transfer of genetic material via phage); (b) transformation (gene transfer via naked DNA); or (c) conjugation (transfer requiring direct contact between the bacteria). Within this category there are two elements that are self-transferable: plasmids and transposons (Tillotson and Watson, 2001).

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