Gram -negative bacteria antibiotic resistance

Resistance has been reported so far in only a few enterococci isolated from immunocompromised patients treated with linezolid for long periods. The resistant isolates appeared to possess modified ribosomal RNA genes. Cross-resistance to other antibiotics has not yet been seen. Most Gram-negative bacteria are resistant by virtue of possessing membrane efflux pumps, but many obligate anaerobes are susceptible. 

The combined intrinsic activities of different efflux pumps play a major role for the intrinsic resistance of Gram-negative bacteria to macrolides and oxazolidi-nones as well as to the intrinsic resistance of Pseudomonas aeruginosa against a broad range of disinfectants and antibiotics. 

Resistance to trimethoprim can be due to the acquisition of plasmid encoded non-allelic variants of the chromosomal DHFR enzyme that are antibiotic unsusceptible. The genes may be part of transposons that then insert into the chromosome. For instance, in gram-negative bacteria the most widespread gene is dhfrl on transposon Tn7. 

Kanamycin (a complex of three antibiotics. A, B and C) is active in low concentrations against various Gram-positive (including penicillin-resistant staphylococci) and Gram-negative bacteria. It is a recognized second-line dmg in the treatment of tuberculosis. 

Gram-negative bacteria are intrinsically resistant to low levels of fusidic acid (a steroid) due to exclusion by the outer membrane. Nevertheless, acquired resistance does occur which has the effect of increasing the level of resistance to the antibiotic. Acquired resistance also occurs in Gram-positive bacteria normally susceptible to fusidic acid. 

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. 

ESR spectra indicated that ultrasound enhanced the penetration of 16-DS into the structurally stronger sites of the inner and outer cell membranes. The effect of ultrasound on the cell membranes was transient in that the initial membrane permeability was restored upon termination of the ultrasound treatment. These results suggested that the resistance of gram-negative bacteria to the action of hydrophobic antibiotics was caused by a low permeability of the outer cell membranes and that this resistance may be reduced by the simultaneous application of antibiotic and ultrasound. 

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