as mechanical ventilators , central venous catheters , and urinary catheters ), plus additional risk factors such as recent antibiotic use and a prior history of having been colonized by or contracted an infection by a multidrug-resistant organism ( MDRO ).”
Shannon explained the process of the escalation of antibiotic resistance .
“ Say we have a patient who needs to be treated for an infection , so we give them an antibiotic ,” he says . “ But the bacteria causing that infection are like , ‘ I ’ m a little too smart for that . I ’ m going to develop resistance .’ So , then the physicians are like , ‘ OK , we need to use a strong antibiotic .’ Then the bacteria say , ‘ I ’ m going to develop strong resistance .’ So , then the physicians are like , ‘ Well , that ’ s fine , we ’ ve got a stronger antibiotic .’ But the pathogens are smarter than us , and they ’ re like , ‘ Yeah , but have you heard of stronger resistance ? Because I got it and I ’ m bringing it .’ Then it takes out our stronger antibiotic . That leaves us with our strongest antibiotics that we have available on the market . And unfortunately , this is the scenario that we ’ re seeing today , especially carbapenemase-producing organisms and some potential for colistin-resistant pathogens as well . So , it ’ s getting scary that we could be running out of effective antibiotics .”
Shannon said that there are several methods of acquiring resistance . Intrinsic resistance is when bacteria are innately resistant to the antibiotic ’ s mechanism of action . Acquired resistance involves vertical gene transfer that occurs during bacterial replication . Horizontal gene transfer can occur via conjugation ( cell-to-cell transfer ), transduction via bacteriophage activity , and transformation ( via free floating DNA ).
“ Those of us in infection prevention are far more worried about acquired resistance ,” Shannon noted . “ Bacteria replicate and pass their genes from cell to cell . We also need to know that there are five different mechanisms of resistance — antibiotic target changes , cell process changes , porin mutation , efflux pumps , and enzymatic inhibition . Germs can develop new cell processes that avoid using the antibiotic ’ s target . They can change or destroy the antibiotics with enzymes , which are proteins that break down the drug . Germs can also restrict access by changing the entryways or limiting the number of entryways . They can change the antibiotic ’ s target so the drug can no longer do its job , and they can get rid of antibiotics by using pumps , much like a sump pump operates in your basement if it gets flooded .”
Shannon then switched gears to discuss laboratory methods and interpretation .
“ We start with the culture ,” he explained . “ Whenever we have a culture , we need to do a susceptibility test . When you get the results , you ’ ll see the minimum inhibitory concentration ( MIC ), which is the lowest concentration of an antibiotic needed to inhibit the growth of bacteria . It may work , it may not work , it ’ s pretty solid , but it ’ s not an exact science ,” Shannon said . “ The breakpoint interpretation of the numbers will be determined by the clinical laboratory , so for example , an 8 might be resistant , but a 2 is susceptible . They will help determine what those breakpoints are specific to each drug-and-bug combo , and so we want to make sure that we ’ re interpreting those appropriately . There are other test options , including phenotypic tests and molecular tests . Many clinical labs are phasing out these kinds of tests in favor of moving directly to genetic testing like PCR testing , which can identify enzymatic inhibition by ESBLs or carbapenemases like Klebsiella pneumoniae carbapenemase ( KPC ), New Delhi metallo beta lactamase ( NDM ) or Oxacillinase-48 ( OXA-48 ), among others .”
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