AntiMicrobial Resistance

intrinsic resistance → natural resistant to certain antibiotics due to pathogen structure and characteristics

acquired resistance → resistance through mutation leading to spread of genes.

Mechanisms of resistance

mutation: spontaneous genetic changed that pass along

horizontal gene transfer - transfer of resistance genes between bacteria

→ they both cause rapid spread of resistance genes so strict control is necessary

  • bacteria use efflux pumps to expel antibiotics from cell to reduce intracellular concentration making efflux pump inhibitors necessary so antibiotics are not affected

  • changes in permeability in bacterial cell wall reduces antibiotic uptake so higher doses are required or alternatives so therapeutic effect is achieved.

  • bacteria are protected by biofilm so antibiotics cant enter or host immune system cannot tackle - higher doses, combination therapy or even physical removal is required

Implications on treatment (enzyme degradation)

  • extended spectrum beta lactamases (ESBLs) break down into beta lactam antibiotics = ineffective. Therefore beta lactamase inhibitors are required like clavulanic acid with hygiene/infection control measures to manage spread

  • carbapenemases breaks down beta lactam antibiotics so use of meropenem-vaborbactam is needed with rigorous infection control

  • MRSA alters penicillin binding proteins which reduces the binding affinity of beta lactam antibiotics so vancomycin and linezolid is required with strict infection control

  • VRE needs linezolid with enhanced infection control to tackle

  • consequences: prolonged illness, mortality and higher costs to tackle harder to treat conditions → longer hospital stays, medication and complicated comorbidities.