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Acquired Resistance

Acquired resistance is said to occur when a particular microorganism obtains the ability to resist the activity of a particular antimicrobial agent to which it was previously susceptible. This can result from the mutation of genes involved in normal physiological processes and cellular structures, from the acquisition of foreign resistance genes or from a combination of these two mechanisms.   

Unlike intrinsic resistance, traits associated with acquired resistance are found only in some strains or subpopulations of each particular bacterial species.  Laboratory methods are therefore needed to detect acquired resistance in bacterial species that are not intrinsically resistant. These same methods are used for monitoring rates of acquired resistance as a means of combating the emergence and spread of acquired resistance traits in pathogenic and non-pathogenic bacterial species.  Acquired resistance results from successful gene change and/or exchange that may involve:  mutation or horizontal gene transfer via transformation, transduction or conjugation.



Table 2.3  Examples of acquired resistance through mutation and horizontal gene transfer





Mycobacterium tuberculosis resistance to rifamycins

Point mutations in the rifampin-binding region of rpoB

Resistance of many clinical isolates to luoroquinolones

Predominantly mutation of the quinolone-resistance-determining-regiont (QRDR) of GyrA and ParC/GrlA

E.coli, Hemophilius influenzae resistance to trimethoprim

Mutations in the chromosomal gene specifying dihydrofolate reductase

Horizontal gene transfer

Staphylococcus aureus resistance to methicillin (MRSA)

Via acquisition of mecA genes which is on a mobile genetic element called “staphylococcal cassette chromosome” (SCCmec) which codes for penicllin binding proteins (PBPs) that are not sensitive to ß-lactam inhibition

Resistance of many pathogenic bacteria against sulfonamides

Mediated by the horizontal transfer of foreign folP genes or parts of it

Enterococcus faecium and E. faecalis resistance to vancomycin

Via acquisition of one of two related gene clusters VanA and Van B, which code for enzymes that modify peptidoglycan precursor, reducing affinity to vancomycin.



Antibiotics exert selective pressure on bacterial populations, killing susceptible bacteria while allowing strains with resistance to that particular antibiotic to survive and multiply.   Traits for such resistance are then vertically passed on to daughter cells, subsequently creating a resistant population which can then spread and be further sources of resistance genes for other strains. 

Because resistance traits are not naturally eliminated or reversed, resistance to a variety of antibiotics may be accumulated over time.  This can lead to strains with multiple drug resistance, which are more difficult to kill due to reduced treatment options.



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