∞ generated and posted on 2016.01.12 ∞
Presence of innate or acquired means by which bacteria avoid the cytotoxic impact of antibacterial chemotherapeutic agents.
|Anything that is Antibiotic Resistant is not harmed (much) by amounts of antibiotic that can be used without hurting a patient.|
Such resistance to antibiotics can be a consequence of either an innate lack of (such as a lack of cell walls in Mycoplasma bacteria), an also innate inability of antibiotics to penetrate to targets (as is seen with antibiotics that are unable to penetrate through, for example, the Gram-negative outer membrane), mutations in the genes encoding antibiotic targets, or acquisition of antibiotic-resistance genes as carried by resistance plasmids. In any case the result is a limitation on the spectrum of activity displayed by the antibiotic such that it is not effective against a given bacterial strain or species.
Mechanisms of antibiotic resistance, especially as associated with resistance plasmids, include enzymatic inactivation of a drug and rapid efflux. Also important, as noted above, is prevention of antibiotic penetration to target site – most notably β-lactamase enzymes – along with mutational modifications of antibiotic targets. Bacteria formation into biofilms also is associated with at least transient resistance to antibiotics as well as disinfectants, as too is bacteria entrance into stationary phase.
Resistance can be (i.e., the result of a specific to adapt a counterattack mechanism against an antibiotic or ) or (where resistance is a consequence of general adaptive processes that are not necessarily linked to a given class of antibiotic; e.g., the nonspecific barrier afforded by the outer membrane of Gram-negative bacteria). Bacteria achieve active drug resistance through three major mechanisms: (1) of the antibiotic from the cell via a collection of membrane-associated ; (2) modification of the antibiotic target (e.g., through mutation of key binding elements such as ribosomal RNA or even by reprogramming of such as in resistance to the ); and (3) via the synthesis of that selectively target and destroy the activity of antibiotics. All of these mechanisms require new by the cell in response to the presence of antibiotics. In fact, in several cases, the antibiotics or their action actually genetically regulate the expression of . Therefore, expend a considerable amount of energy and to actively resist antibiotics.