Bacteria resistance mechanisms

Development of Resistance. One of the principal disadvantages of sulfonamide therapy is the emergence of dmg-resistant strains of bacteria. Resistance develops by several mechanisms overproduction of PABA (38) altered permeabiUty of the organisms to sulfonamides (39) and reduced affinity of dihydropteroate synthetase for sulfonamides while the affinity for PABA is retained (40). Sulfonamides also show cross-resistance to other sulfonamides but not to other antibacterials. In plasmodia, resistance may occur by means of a bypass mechanism in which the organisms can use preformed foHc acid (41). 

The presence of a specific resistance mechanism in a bacterial isolate does not necessarily implicate that this isolate is resistant in clinical terms. However, an isolate expressing a resistance mechanism possibly will be eliminated less easily as compared to a susceptible one. In clinical practice, resistance mechanisms will be rarely identified. Usually the sensitivity of isolates will be determined and reported to the clinician by using the interpretive criteria which is sensitive, intermediate or resistant. Some bacteria harbouring resistance... 

A third resistance mechanism is akin to that described for the AGAC antibiotics and chloramphenicol, whereby changes in the outer membrane porins of Gram-negative bacteria reduce the penetration of /3-lactams resulting in low levels of resistance. 

Table 13.4 Examples of intrinsic resistance mechanisms to biocides in bacteria...

Some metals can be converted to a less toxic form through enzyme detoxification. The most well-described example of this mechanism is the mercury resistance system, which occurs in S. aureus,43 Bacillus sp.,44 E. coli,45 Streptomyces lividans,46 and Thiobacillus ferrooxidans 47 The mer operon in these bacteria includes two different metal resistance mechanisms.48 MerA employs an enzyme detoxification approach as it encodes a mercury reductase, which converts the divalent mercury cation into elemental mercury 49 Elemental mercury is more stable and less toxic than the divalent cation. Other genes in the operon encode membrane proteins that are involved in the active transport of elemental mercury out of the cell.50 52... 

The mechanism of Ag(I) cytotoxicity is unknown. Cell wall damage may be important and it has been shown that Cys-150 in the enzyme phosphomannose isomerase, an essential enzyme for the biosynthesis of Candida albicans cell walls, is the Ag(I) target in this organism (330). Silver resistant bacteria are known, but only recently has significant progress been made in understanding the resistance mechanisms (637). 

Table 1 Examples of action and resistance mechanisms found in bacteria for different classes of antibacterial agents ...

Two mechanisms of resistance have been discovered with respect to fluoroquinolones a change in subunits A of DNA-gyrase, and reduced permeability of the outer membrane of the bacteria. Resistance is mediated by chromosomes, and not plasmids in the bacteria. The development of resistance while using the drugs is very rarely observed. 

Tigecycline IV unaffected by common tetracycline resistance mechanisms very broad spectrum of activity against grampositive, gram-negative, and anaerobic bacteria nausea and vomiting are the primary toxicities... 

The aim of the this section is to describe some specific resistant mechanisms of bacteria against cephalosporin antibiotics focusing on /3-lactamase action and the interaction of cephalosporins with penicillin binding proteins (PBPs). 

Bacteria can obtain the various types of resistance mechanisms described previously by undergoing modifications in their genetic constitution. Many bacteria simply inherit their resistance genes from their forerunners. In addition, genetic mutations can occur that can confer a new trait. For example, it has been estimated that bacteria undergo spontaneous mutation at a frequency of approximately 1 in 10 cells. These mutations can confer resistant traits to the subsequent progeny. Mutations are believed... 

A knowledge of the site and action of antibacterial agents is important in understanding at least some of the resistance mechanisms presented by bacteria. 

Multidrug resistance (Mdr) is a serious problem in enteric and other Gramnegative bacteria [41, 71, 273-283] (Table 4.17). As distinct from plasmid-mediated resistance, described above, Mdr is a term employed to describe a resistance mechanism by genes that comprise part of the normal cell genome. These genes are activated by induction or mutation caused by some types of stress, considered below. Because the genes are ubiquitously distributed, there is no need for genetic transfer. 

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